Donata Vercelli

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Chapters

• DeVries, A., & Vercelli, D. (2022). Epigenetics of Allergies. In Epigenetics of the Immune System. Elsevier.
• Vercelli, D. (2022). Inherited susceptibility to complex diseases. In Comprehensive Toxicology, 3rd Edition.
• Vercelli, D. (2017). Inherited susceptibility to complex diseases. In Comprehensive Toxicology. Elsevier.
• DeVries, A., & Vercelli, D. (2016). DNA Methylation Biomarkers in Asthma and Allergy. In Epigenetic Biomarkers and Diagnostics. Elsevier Inc. doi:10.1016/b978-0-12-801899-6.00017-6
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  The role of epigenetic processes, primarily DNA methylation, in allergic disease susceptibility and severity is actively explored because of the inability of genetic factors to explain more than a small proportion of the variance in disease phenotype and the functional link among epigenetic mechanisms, environmental exposures, and developmental programs. To date, a number of genome-wide and candidate-gene DNA methylation studies have been performed in populations with asthma, allergic rhinitis, or atopic dermatitis, focusing not only on peripheral blood but also on airway tissue and lesional skin. Differential DNA methylation was detected at biologically plausible loci, but these initial studies should be considered exploratory because of potential issues with population design, size, and phenotypic heterogeneity. Studies leveraging DNA methylation data as clinical biomarkers are also beginning. Future work in longitudinal mother-child birth cohorts will likely highlight the contribution that methylome screens can give to the clinical management of allergic disease and unveil the role played by epigenetic mechanisms in allergic disease pathogenesis.
• Vercelli, D., & DeVries, A. (2016). DNA methylation biomarkers in asthma and allergy. In Epigenetic Biomarkers and Diagnostics(pp 331-350). Academic Press.
• Vercelli, D. (2006). Interleukin-13. In Genetics of Asthma and Chronic Obstructive Pulmonary Disease. CRC Press.
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  Few genes appear to be as critical for the pathogenesis of allergic inflammation in humans and animal models as interleukin (IL)-13, and even fewer appear to determine susceptibility to allergy and Asthma across human populations as consistently as IL-13. The reason behind the central role of this cytokine in disease pathogenesis probably lies in the properties of IL-13, the frequency with which the human IL-13 locus is targeted by natural genetic variation, and the functional consequences of this variation. Here we will discuss the properties of IL-13 relevant to allergic lung inflammation; we will review the results of genetic association studies investigating the relationship between IL-13 polymorphisms and allergic phenotypes; and we will propose a blueprint for functional studies of genetic variation based on the experience gained through the analysis of a common IL-13 coding variant.
• Cameron, L., & Vercelli, D. (2005). Regulation of IgE synthesis. In Asthma Prevention. CRC Press. doi:10.1201/b14148-31
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  This chapter addresses the cellular and molecular mechanisms of IgE regulation. The signals that trigger IgE synthesis are outlined and followed by a detailed description of the molecular events that such interactions induce. Over the past few decades, this molecular approach has allowed immunologists to understand the basic mechanisms of isotype switching to IgE. Finally, potential therapeutic targets of the molecular process of IgE regulation are discussed.

Journals/Publications

• Agache, I., Balbin-Ramon, G. J., Saenz, F. K., Sola-Arnau, I., Alonso-Coello, P., Haahtela, T., Traidl-Hoffmann, C., O'Mahony, L., Damialis, A., Lauerma, A., Nadeau, K. C., Pali-Schöll, I., Palomares, O., Renz, H., Schwarze, J., Vercelli, D., Canelo-Aybar, C., Jutel, M., & Akdis, C. A. (2025). Impact of Residential Greeness Exposure on the Development of Allergic Diseases and Asthma and on Asthma Control-A Systematic Review for the EAACI Guidelines of Environmental Science for Allergic Diseases and Asthma. Allergy, 80(11), 3027-3042.
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  The role of residential greenness exposure (RGE) in prevention and control of allergic diseases remains controversial. This systematic review evaluated the association between RGE and the risk of developing asthma, allergic rhinitis (AR), food allergy, atopic dermatitis (AD), and asthma control. MEDLINE and EMBASE searches retrieved 17 cohort and case-control longitudinal studies (12 for asthma, 6 AR, 1 food allergy, 1 ad). Risk of bias was assessed with ROBINS-E, and certainty of evidence with GRADE. Data were meta-analyzed using adjusted odds ratios (aORs) with random-effects models. For "ever asthma" and "ever AR" a non-significant protective trend of RGE was observed (aOR 0.92, 95% CI 0.72-1.18; aOR 0.61; 95% CI 0.24-1.55). For "current asthma" RGE was associated with increased risk (aOR 1.17, 95% CI 1.04-1.33), with no clear association for "current AR" (aOR 1.03; 95% CI 0.80-1.32). Prenatal RGE reduced the risk of "ever asthma" (aOR 0.94, 95% CI 0.93-0.950) and AD (aOR 0.996, 95% CI 0.993-0.999). RGE increased the risk for peanut (aOR 1.78, 95% CI 1.13-2.82) and egg allergy (aOR 1.38, 95% CI [1.05-1.82]). Reduced RGE decreased asthma control (OR: 2.662, 95% CI [1.043-6.799]). Potential benefits or potential harms of RGE should be judged in a context-specific manner.
• Agache, I., Salazar, J., Rodriguez-Tanta, Y., Saenz, F. K., Haahtela, T., Traidl-Hoffmann, C., Damialis, A., Vecillas, L., Giovannini, M., Nadeau, K. C., Pali-Schöll, I., Palomares, O., Renz, H., Schwarze, J., Sousa Pinto, B., Urrutia-Pereira, M., Venter, C., Vercelli, D., Winders, T., , Sola-Arnau, I., et al. (2025). The Impact of Rhinovirus, Syncytial Respiratory Virus and Helminth Infection on the Risk of New-Onset Asthma and Other Allergic Conditions-A Systematic Review for the EAACI Guidelines on Environmental Science for Allergic Diseases and Asthma. Allergy, 80(7), 1878-1898.
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  This systematic review evaluated the association between lower respiratory tract infections (LRTI) in infancy with respiratory syncytial virus (RSV), rhinovirus (RV) or infestation with helminths and the risk of developing asthma and allergic diseases. The risk of bias was assessed with ROBINS-E, and the certainty of evidence (CoE) with GRADE. Meta-analysis applied a random-effects model. RSV LRTI is likely associated with an increased risk of developing asthma by age 7 (OR 3.02, 95% CI 2.23-4.09; I = 98%; moderate CoE). The impact on wheezing, atopic dermatitis (AD), and allergic rhinitis is uncertain. RV LRTI may be associated with increased risk of developing asthma (OR 8.40, 95% CI 2.56-27.55; I = 43%; low CoE). The impact on wheezing and AD is uncertain. Trichuris trichiura infestation might be associated with reduced risk of new-onset wheezing (OR 0.57, 95% CI 0.35-0.94; very low CoE) or AD (HR: 0.35, 95% CI 0.18-0.67; very low CoE). The association between Ascaris lumbricoides and hookworm infestation and the risk of developing asthma or AD is uncertain. Infestation with any helminths might be associated with reduced risk of new-onset asthma by age 5 (OR: 0.60, 95% CI 0.38-0.95; very low CoE) and wheezing (OR 0.70, 95% CI 0.51-0.95; very low CoE). More high-quality studies are needed to confirm these findings.
• DeVries, A., Kimura, H., Kimura, N., Molzahn, A., Pivniouk, V., Ledford, J. G., Numata, M., Chu, H. W., Vercelli, D., & Kraft, M. (2025). Asthma programs the transcriptional response of human nasal epithelial cells to SARS-CoV-2 Spike-mediated ACE2 engagement. The Journal of allergy and clinical immunology, 156(5), 1430-1432.e4.
• DeVries, A., Kimura, H., Kimura, N., Molzahn, A., Pivniouk, V., Ledford, J. G., Numata, M., Chu, H. W., Vercelli, D., & Kraft, M. (2025). Asthma programs the transcriptional response of human nasal epithelial cells to SARS-CoV-2 Spike-mediated ACE2 engagement. The Journal of allergy and clinical immunology, 156(Issue 5). doi:10.1016/j.jaci.2025.07.007
• Grigg, J., Barratt, B., Bønnelykke, K., Custovic, A., Ege, M., Pasquali, C., Palomares, O., Shaheen, S., Sokolowska, M., Vercelli, D., Maizels, R., & von Mutius, E. (2025). European Respiratory Society Research Seminar on Preventing Pediatric Asthma. Pediatric pulmonology, 60(1), e27401.
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  This report is a summary of the presentations given at the European Respiratory Society's Research Seminar on Asthma Prevention. The seminar reviewed both epidemiological and mechanistic studies and concluded that; (i) reducing exposure of pregnant women and children to air pollution will reduce incident asthma, (ii) there are promising data that both fish oil and a component of raw cow's milk prevent asthma, and (iii) modulating trained immunity by either mimicking helminth infection or oral and sublingual bacterial products is a promising area of research.
• Haahtela, T., O'Mahony, L., Traidl-Hoffmann, C., Akdis, M., Ceylan, O., Chaslaridis, P., Damialis, A., Del Giacco, S., Lauerma, A., Nadeau, K. C., Paciência, I., Pali-Schöll, I., Palomares, O., Renz, H., Schwarze, J., Urrutia-Pereira, M., Venter, C., Vercelli, D., Winders, T., , Akdis, C. A., et al. (2025). EAACI Guidelines on the Importance of Green Space in Urban Environments for Allergy and Asthma Prevention. Allergy.
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  The allergy and asthma epidemic in urban societies following World War II is mostly caused by changes in the environment, diet and lifestyle. Disconnection of urban populations from the wider environment has reduced the protective factors building up immunological resilience. The European Academy of Allergy and Clinical Immunology (EAACI) guidelines on greenness impact on allergy and asthma follow the Grading of Recommendations, Assessment, Development and Evaluation (GRADE) approach and provide eight recommendations encouraging greenness exposure to support immune health. Controlled follow-up studies are still scarce, and the strength of evidence is generally low or moderate at best. For primary prevention of allergy and asthma, most of the evidence indicates beneficial effects. Exposure is also useful for secondary prevention. Asthma patients may feel better and need less medication by combining green space exposure with physical activity. During the high-pollen season, effective seasonal medication is necessary for patients with pollen allergy. In urban planning, implementing appropriate green infrastructure and easy access to green space promotes immune health and reduces risks of air pollution and heatwaves. These EAACI guidelines are the first recommendations highlighting the importance of urban green spaces on immune health and call for prioritising innovative research in this field.
• Nouri, H. R., Schaunaman, N., Kraft, M., Numata, M., Vercelli, D., & Chu, H. W. (2025). Tollip deficiency enhances mitophagy and reduces STING activation in influenza A virus–infected mice. Journal of Immunology, 214(Issue 7). doi:10.1093/jimmun/vkaf058
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  Toll-interacting protein (Tollip) is an intracellular adaptor protein with diverse functions including regulation of autophagy of mitochondria—mitophagy. Tollip deficiency promotes viral infection, but whether mitophagy is involved remains unclear. We sought to determine if mitophagy and associated signaling such as mitochondrial DNA (mtDNA) release and activation of stimulator of interferon genes (STING) contribute to worsened viral infection due to Tollip deficiency. Wild-type and Tollip knockout (KO) C57/BL6 mice were intranasally infected with influenza A virus (IAV), and then treated with or without a STING agonist 2'3'cGAMP for 4 d. PINK1 (an initiator of mitophagy) KO mouse tracheal epithelial cells (mTECs) or PINK1 KO mice were infected with IAV to reveal the role of mitophagy in viral infection. In IAV-infected mice, Tollip deficiency enhanced lung mitophagy (more PINK1 and BNIP3L, but less p62), and decreased release of mtDNA. Furthermore, Tollip deficiency suppressed STING activation and the antiviral response (eg IFN-β and MX1), and increased viral load. In IAV-infected Tollip KO mice, 2'3'cGAMP activated STING and increased antiviral response coupled with less virus. PINK1-deficient mice increased lung release of mtDNA and augmented STING activation and antiviral responses. PINK1 deficiency in mTECs increased STING activation and significantly decreased the viral load. Our findings suggest that enhanced mitophagy due to Tollip deficiency reduces mtDNA release and STING activation during viral infection, resulting in decreased antiviral responses. Reduction of mitophagy and/or STING activation may open novel avenues for therapeutic intervention in human subjects with Tollip deficiency and viral infection.
• Pivniouk, V., Pivniouk, O., Uhrlaub, J. L., Hahn, S., Molzahn, A., Kimura, H., Numata, M., Chu, H. W., Ledford, J. G., Kraft, M., Nikolich, J. Ž., & Vercelli, D. (2025). IL-13 protects epithelial cells from SARS-CoV-2 infection by inhibiting ACE2-mediated virus binding and cell entry. ImmunoHorizons, 9(12).
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  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) preferentially infects airway epithelial cells. This infection is mediated by the binding of SARS-CoV-2 spike (S) protein to ACE2 expressed on target cells. Patients with allergic (type-2) asthma have been reported to be less susceptible to coronavirus disease 2019 (COVID-19), but these effects are controversial and mechanistically unclear. We previously showed lower expression of ACE2 mRNA in airway epithelial cells from type-2 asthmatics compared to healthy donors. Moreover, we and others demonstrated that the type-2 cytokine interleukin 13 (IL-13) suppresses ACE2 expression and SARS-CoV-2 infection in human epithelial cells. To better understand the relationship between type-2 inflammation, ACE2 expression, and SARS-CoV-2 infection, we investigated the effects of IL-13 on critical steps of epithelial cell infection by SARS-CoV-2: S protein-mediated binding to ACE2 on epithelial cells, and ACE2-mediated SARS-CoV-2 entry into these cells. Recombinant IL-13 significantly inhibited both these processes. This inhibition appeared to be mediated by IL-13-induced suppression of ACE2 transcription because IL-13 failed to affect S protein-mediated viral entry into cells that express ACE2 under the control of an IL-13 unresponsive heterologous promoter. We propose that IL-13 protects epithelial cells from SARS-CoV-2 infection largely by inhibiting ACE2 expression and ACE2-mediated downstream events that allow the virus to access its cellular targets.
• Michael, A. N., Pivniouk, O., Ezeh, P. C., Banskar, S., Hahn, S., DeVries, A., O'Connell, K., Pivniouk, V., & Vercelli, D. (2024). Administration of a bacterial lysate to the airway compartment is sufficient to inhibit allergen-induced lung eosinophilia in germ-free mice. Journal of leukocyte biology, 116(2), 392-397.
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  The nexus between eosinophils and microbes is attracting increasing attention. We previously showed that airway administration of sterile microbial products contained in dust collected from traditional dairy farms virtually abrogated bronchoalveolar lavage (BAL) eosinophilia and other cardinal asthma phenotypes in allergen-sensitized specific pathogen-free (SPF) mice. Interestingly, comparable inhibition of allergen-induced BAL eosinophilia and promotion of airway barrier integrity were found upon administration of a sterile, pharmacological-grade bacterial lysate, OM-85, to the airway compartment of allergen-sensitized SPF mice. Here, we asked whether intrinsic properties of airway-delivered microbial products were sufficient to inhibit allergic lung inflammation or whether these effects were mediated by reprogramming of the host microbiota. We compared germ-free (GF) mice and offspring of GF mice associated with healthy mouse gut microbiota and maintained under SPF conditions for multiple generations (Ex-GF mice). These mice were treated intranasally with OM-85 and evaluated in the ovalbumin and Alternaria models of allergic asthma focusing primarily on BAL eosinophilia. Levels of allergen-induced BAL eosinophilia were comparable in GF and conventionalized Ex-GF mice. Airway administration of the OM-85 bacterial lysate was sufficient to inhibit allergen-induced lung eosinophilia in both Ex-GF and GF mice, suggesting that host microbiota are not required for the protective effects of bacterial products in these models and local airway exposure to microbial products is an effective source of protection. OM-85-dependent inhibition of BAL eosinophilia in GF mice was accompanied by suppression of lung type 2 cytokines and eosinophil-attracting chemokines, suggesting that OM-85 may work at least by decreasing eosinophil lung recruitment.
• Vercelli, D. (2024). IL-4 and dendritic cells in atopic dermatitis: Old dogs learn new tricks. Journal of Allergy and Clinical Immunology, 154(6). doi:10.1016/j.jaci.2024.10.001
• Vercelli, D. (2024). IL-4 and dendritic cells in atopic dermatitis: Old dogs learn new tricks. The Journal of allergy and clinical immunology, 154(6), 1419-1421.
• Vercelli, D., & Galli, S. (2024). The origins, manifestations, and potential treatments of allergic disorders. Seminars in Immunology, 73(Issue). doi:10.1016/j.smim.2024.101886
• Vercelli, D., & Galli, S. J. (2024). The origins, manifestations, and potential treatments of allergic disorders. Seminars in immunology, 73, 101886.
• Xing, Y., Tsang, M. S., Yang, Z., Wang, M. H., Pivniouk, V., Leung, A. S., Leung, T. F., Roponen, M., Schaub, B., Vercelli, D., Wong, C. K., Li, J., & Wong, G. W. (2024). Immune modulation by rural exposures and allergy protection. Pediatric allergy and immunology : official publication of the European Society of Pediatric Allergy and Immunology, 35(2), e14086.
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  Growing up on traditional farms protects children from the development of asthma and allergies. However, we have identified distinct asthma-protective factors, such as poultry exposure. This study aims to examine the biological effect of rural exposure in China.
• Xing, Y., Tsang, M. S., Yang, Z., Wang, M. H., Pivniouk, V., Leung, A. S., Leung, T., Roponen, M., Schaub, B., Vercelli, D., Wong, C., Li, J., & Wong, G. W. (2024). Immune modulation by rural exposures and allergy protection. Pediatric Allergy and Immunology, 35(2). doi:10.1111/pai.14086
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  Background: Growing up on traditional farms protects children from the development of asthma and allergies. However, we have identified distinct asthma-protective factors, such as poultry exposure. This study aims to examine the biological effect of rural exposure in China. Methods: We recruited 67 rural children (7.4 ± 0.9 years) and 79 urban children (6.8 ± 0.6 years). Depending on the personal history of exposure to domestic poultry (DP), rural children were further divided into those with DP exposure (DP+, n = 30) and those without (DP−, n = 37). Blood samples were collected to assess differential cell counts and expression of immune-related genes. Dust samples were collected from poultry stables inside rural households. In vivo activities of nasal administration of DP dust extracts were tested in an ovalbumin-induced asthma model. Results: There was a stepwise increase in the percentage of eosinophils (%) from rural DP+ children (median = 1.65, IQR = [1.28, 3.75]) to rural DP− children (3.40, [1.70, 6.50]; DP+ vs. DP−, p =.087) and to the highest of their urban counterparts (4.00, [2.00, 7.25]; urban vs. DP+, p =.017). Similarly, rural children exhibited reduced mRNA expression of immune markers, both at baseline and following lipopolysaccharide (LPS) stimulation. Whereas LPS stimulation induced increased secretion of Th1 and proinflammatory cytokines in rural DP+ children compared to rural DP− children and urban children. Bronchoalveolar lavage of mice with intranasal instillation of dust extracts from DP household showed a significant decrease in eosinophils as compared to those of control mice (p
• Marques dos Santos, M., Pivniouk, V., Rankl, B., Walker, A., Pagani, G., Hertkorn, N., Schmitt-Kopplin, P., Müller, C., Bracher, F., Merl-Pham, J., Hauck, S. M., Schloter, M., Michael, A. N., Anderson, D., Honeker, L., Gozdz, J., Pivniouk, O., Ober, C., Holbreich, M., , Martinez, F. D., et al. (2023). Asthma-protective agents in dust from traditional farm environments. Journal of Allergy and Clinical Immunology, 152(Issue 3). doi:10.1016/j.jaci.2023.05.013
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  Background: Growing up on traditional European or US Amish dairy farms in close contact with cows and hay protects children against asthma, and airway administration of extracts from dust collected from cowsheds of those farms prevents allergic asthma in mice. Objectives: This study sought to begin identifying farm-derived asthma-protective agents. Methods: Our work unfolded along 2 unbiased and independent but complementary discovery paths. Dust extracts (DEs) from protective and nonprotective farms (European and Amish cowsheds vs European sheep sheds) were analyzed by comparative nuclear magnetic resonance profiling and differential proteomics. Bioactivity-guided size fractionation focused on protective Amish cowshed DEs. Multiple in vitro and in vivo functional assays were used in both paths. Some of the proteins thus identified were characterized by in-solution and in-gel sodium dodecyl sulfate–polyacrylamide gel electrophoresis enzymatic digestion/peptide mapping followed by liquid chromatography/mass spectrometry. The cargo carried by these proteins was analyzed by untargeted liquid chromatography–high-resolution mass spectrometry. Results: Twelve carrier proteins of animal and plant origin, including the bovine lipocalins Bos d 2 and odorant binding protein, were enriched in DEs from protective European cowsheds. A potent asthma-protective fraction of Amish cowshed DEs (≈0.5% of the total carbon content of unfractionated extracts) contained 7 animal and plant proteins, including Bos d 2 and odorant binding protein loaded with fatty acid metabolites from plants, bacteria, and fungi. Conclusions: Animals and plants from traditional farms produce proteins that transport hydrophobic microbial and plant metabolites. When delivered to mucosal surfaces, these agents might regulate airway responses.
• Vercelli, D., & Lynch, S. V. (2023). Interactions between host epigenetics and microbiota: Who does what to whom, when, and why?. Journal of Allergy and Clinical Immunology, 151(Issue 6). doi:10.1016/j.jaci.2023.01.018
• DeVries, A. A., McCauley, K., Stern, D. A., Lynch, S. V., & Vercelli, D. (2021). Maternal prenatal immunity, neonatal immune training, and early airway microbiota development shape the trajectory to childhood asthma. PNAS.
• DeVries, A., & Vercelli, D. (2016). Epigenetics and the trajectory to asthma. Epigenomics.
• Long, X., Daya, M., Zhao, J., Rafaels, N., Liang, H., Potee, J., Campbell, M., Zhang, B., Araujo, M., Oliveira, R., Mathias, R., Gao, L., Ruczinski, I., Georas, S., Vercelli, D., Beaty, T., Barnes, K., Chen, X., & Chen, Q. (2016). The role of ST2 and ST2 variants in schistosomiasis. J. Allergy Clin. Immunol..
• Pali-Schöll, I., Vercelli, D., Jensen-Jarolim, E., & von Mutius, E. (2021). Completing the hygiene hypothesis: secretory protein beta-lactoglobulin in stable dust may contribute to the allergy protective effect of cattle farms. Allergy.
• Vercelli, D., DeVries, A., McCauley, K., Fadrosh, D., Fujimura, K. E., Stern, D. A., & Lynch, S. V. (2022). Maternal prenatal immunity, neonatal trained immunity, and early airway microbiota shape childhood asthma development. Allergy, 77(12), 3617-3628. doi:10.1111/all.15442
• Vercelli, D., Nikolich-Zugich, J., Kraft, M., Anderson, D., Churko, J., Ezeh, P., Malone, S. P., Hahn, S., Conway, M. Y., VanLinden, S. R., Pivniouk, D., Michael, A., Uhrlaub, J. L., DeVries, A., Pivniouk, O., & Pivniouk, V. I. (2021). The OM-85 bacterial lysate inhibits SARS-CoV-2 infection of epithelial cells by downregulating SARS-CoV-2 receptor expression. The Journal of Allergy and Clinical Immunology. doi:10.1016/j.jaci.2021.11.019
• Vercelli, D., Pasquali, C., Martinez, F., DeVries, A., Gozdz, J., Anderson, D., Abidov, A., Pivniouk, O. N., Michael, A., Ezeh, P., Gimenes-Junior, J. A., & Pivniouk, V. I. (2021). Airway administration of OM-85, a bacterial lysate, blocks experimental asthma by targeting dendritic cells and the epithelium/IL-33/ILC2 axis. The Journal of Allergy and Clinical Immunology. doi:10.1016/j.jaci.2021.09.013
• Vercelli, D., Vanlinden, S. R., Uhrlaub, J. L., Pivniouk, V., Pivniouk, O., Pivniouk, D., Nikolich-zugich, J., Michael, A., Malone, S. P., Kraft, M., Hahn, S., Ezeh, P., Devries, A., Conway, M. Y., Churko, J. M., & Anderson, D. (2022). The OM-85 bacterial lysate inhibits SARS-CoV-2 infection of epithelial cells by downregulating SARS-CoV-2 receptor expression.. The Journal of allergy and clinical immunology, 149(3), 923-933.e6. doi:10.1016/j.jaci.2021.11.019
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  Treatments for coronavirus disease 2019, which is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), are urgently needed but remain limited. SARS-CoV-2 infects cells through interactions of its spike (S) protein with angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) on host cells. Multiple cells and organs are targeted, particularly airway epithelial cells. OM-85, a standardized lysate of human airway bacteria with strong immunomodulating properties and an impeccable safety profile, is widely used to prevent recurrent respiratory infections. We found that airway OM-85 administration inhibits Ace2 and Tmprss2 transcription in the mouse lung, suggesting that OM-85 might hinder SARS-CoV-2/host cell interactions..We sought to investigate whether and how OM-85 treatment protects nonhuman primate and human epithelial cells against SARS-CoV-2..ACE2 and TMPRSS2 mRNA and protein expression, cell binding of SARS-CoV-2 S1 protein, cell entry of SARS-CoV-2 S protein-pseudotyped lentiviral particles, and SARS-CoV-2 cell infection were measured in kidney, lung, and intestinal epithelial cell lines, primary human bronchial epithelial cells, and ACE2-transfected HEK293T cells treated with OM-85 in vitro..OM-85 significantly downregulated ACE2 and TMPRSS2 transcription and surface ACE2 protein expression in epithelial cell lines and primary bronchial epithelial cells. OM-85 also strongly inhibited SARS-CoV-2 S1 protein binding to, SARS-CoV-2 S protein-pseudotyped lentivirus entry into, and SARS-CoV-2 infection of epithelial cells. These effects of OM-85 appeared to depend on SARS-CoV-2 receptor downregulation..OM-85 inhibits SARS-CoV-2 epithelial cell infection in vitro by downregulating SARS-CoV-2 receptor expression. Further studies are warranted to assess whether OM-85 may prevent and/or reduce the severity of coronavirus disease 2019.
• Vercelli, D., Wheatley, L. M., Holloway, J. W., Svanes, C., Sears, M. R., Breton, C., Fedulov, A. V., Nilsson, E., Zhang, H., Togias, A., & Arshad, S. H. (2022). The role of epigenetics in multi‐generational transmission of asthma: An NIAID workshop report‐based narrative review. Clinical & Experimental Allergy, 52(11), 1264-1275. doi:10.1111/cea.14223
• Wittek, T., Winkler, S., Widhalm, R., Vercelli, D., Roth-walter, F., Pranger, C., Pali-scholl, I., Pacios, L. F., Mutius, E. V., Mayerhofer, H., Korath, A. D., Kasper-giebl, A., Jensen-jarolim, E., Hufnagl, K., Hofstetter, G., Hann, S., Bianchini, R., Altemeier, T., Ahlers, S., & Afify, S. M. (2022). Secretory protein beta-lactoglobulin in cattle stable dust may contribute to the allergy-protective farm effect.. Clinical and translational allergy, 12(2), e12125. doi:10.1002/clt2.12125
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  Growing up on a cattle farm and consuming raw cow's milk protects against asthma and allergies. We expect a cattle-specific protein as active component in this farm effect..Dust was collected from cattle and poultry stables and from mattresses of households. Urine was obtained from cattle, and ambient aerosols were sampled. Samples were analysed for BLG by SDS PAGE/immunoblot and mass spectrometry, and for association with metals by SEC-ICP-MS. PBMC of healthy donors were incubated with BLG +/- zinc, and proliferation and cytokines determined. BALB/c mice were pre-treated intranasally with stable dust extract containing BLG or depleted of BLG, and subsequent allergy response after sensitization was evaluated on antibody and symptom level..A major protein in dust from cattle farms and ambient air was identified as BLG. Urine from female and male cattle is a major source of BLG. In dust samples, BLG was associated with zinc. In vitro, zinc-BLG provoked significantly lower proliferation of CD4+ and CD8+ cells while inducing significantly higher levels of IFN-γ and IL-6 than the apo-BLG devoid of zinc. In vivo, pre-treatment of mice with dust extract containing BLG resulted in lower allergy symptom scores to BLG and unrelated Bet v 1 than pre-treatment with extract depleted of BLG. These in vitro and in vivo effects were independent of endotoxin..The lipocalin BLG is found in large amounts in cattle urine, accumulates in bovine dust samples and is aerosolized around farms. Its association with zinc favorably shapes the human cellular immune response towards Th1-cytokines in vitro. BLG together with zinc in stable dust protects mice from allergic sensitization. BLG with its associated ligands may in an innate manner contribute to the allergy-protective farm effect.
• Lynch, S. V., & Vercelli, D. (2021). Microbiota, Epigenetics and Trained Immunity: Convergent Drivers and Mediators of the Asthma Trajectory from Pregnancy to Childhood. American journal of respiratory and critical care medicine.
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  The prevalence of allergy and asthma has increased significantly over the past several decades, especially in industrialized nations where environmental exposures and lifestyles have rapidly diverged from those with which humans evolved. Developing effective interventions for precision treatment and prevention of allergy and asthma requires a deeper understanding of their origins and underlying mechanisms. This Perspective proposes a trans-generational framework for future studies that integrates microbiome, immunology, genetics and epigenetics research in human populations and model systems. We suggest that environmental exposures during pregnancy shape maternal microbiomes and immune function, which in turn influence fetal immune and microbiome development in the context of the child's genetic makeup. Relying on epigenetic mechanisms, these interacting influences train the neonate's innate immune system and regulate its ability to respond to the stimuli provided by microbes vertically transmitted from the mother that initially colonize neonatal body habitats. Depending on their composition and functional properties, these pioneer microbes shape immune function which controls the rate and types of exogenous microbes accumulated into these body habitats during the first year of life, thereby determining trajectories of microbiota development, innate and adaptive immune development, and ultimately asthma risk. One critical implication of the framework we propose is that hitherto independent research tracks should converge to determine how very early life microbes in the context of extrinsic and intrinsic factors direct the accumulation of environmental microbes in early life, and how the composition and metabolic capacity of the child's microbiome at various body habitats, shaped by these interacting influences, controls immune development and asthma risk.
• Pivniouk, V., Gimenes-Junior, J. A., Ezeh, P., Michael, A., Pivniouk, O., Hahn, S., VanLinden, S. R., Malone, S. P., Abidov, A., Anderson, D., Gozdz, J., DeVries, A., Martinez, F. D., Pasquali, C., & Vercelli, D. (2021). Airway administration of OM-85, a bacterial lysate, blocks experimental asthma by targeting dendritic cells and the epithelium/IL-33/ILC2 axis. The Journal of allergy and clinical immunology (with Editorial).
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  Microbial interventions against allergic asthma have robust epidemiologic underpinnings and the potential to recalibrate disease-inducing immune responses. Oral administration of OM-85, a standardized lysate of human airways bacteria, is widely used empirically to prevent respiratory infections and a clinical trial is testing its ability to prevent asthma in high-risk children. We previously showed that intranasal administration of microbial products from farm environments abrogates experimental allergic asthma.
• Pivniouk, V., Pivniouk, O., DeVries, A., Uhrlaub, J. L., Michael, A., Pivniouk, D., VanLinden, S. R., Conway, M. Y., Hahn, S., Malone, S. P., Ezeh, P., Churko, J. M., Anderson, D., Kraft, M., Nikolich-Zugich, J., & Vercelli, D. (2021). The OM-85 bacterial lysate inhibits SARS-CoV-2 infection of epithelial cells by downregulating SARS-CoV-2 receptor expression. The Journal of allergy and clinical immunology.
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  Treatments for coronavirus disease 2019, which is caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), are urgently needed but remain limited. SARS-CoV-2 infects cells through interactions of its spike (S) protein with angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) on host cells. Multiple cells and organs are targeted, particularly airway epithelial cells. OM-85, a standardized lysate of human airway bacteria with strong immunomodulating properties and an impeccable safety profile, is widely used to prevent recurrent respiratory infections. We found that airway OM-85 administration inhibits Ace2 and Tmprss2 transcription in the mouse lung, suggesting that OM-85 might hinder SARS-CoV-2/host cell interactions.
• Vercelli, D. (2021). Microbiota and human allergic diseases: the company we keep. Current opinion in immunology, 72, 215-220.
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  Environmental, maternal and early life microbial/immune networks program human developmental trajectories and health outcomes and strongly modify allergic disease risk. The effects of environmental microbiota are illustrated by the 'farm effect' (the protection against asthma and allergy conferred by growing up on a traditional farm) and other natural experiments in populations exposed to microbe-rich environments. The role of gut microbiome maturation in the asthma/allergy trajectory is demonstrated by the most recent farm studies, which identified microbial metabolites specifically associated with asthma protection, and studies in other cohorts, which defined dynamic microbial community profiles associated with allergic disease phenotypes. Current and future studies in germ-free mice associated with gut microbiota from human disease states are providing novel mechanistic insights into the role of microbiota in shaping immune function and allergic disease susceptibility.
• Kimura, H., Francisco, D., Conway, M., Martinez, F. D., Vercelli, D., Polverino, F., Billheimer, D., & Kraft, M. (2020). Type 2 inflammation modulates ACE2 and TMPRSS2 in airway epithelial cells. Journal of Allergy and Clinical Immunology, 146(Issue 1). doi:10.1016/j.jaci.2020.05.004
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  Background: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has dramatically changed our world, country, communities, and families. There is controversy regarding risk factors for severe COVID-19 disease. It has been suggested that asthma and allergy are not highly represented as comorbid conditions associated with COVID-19. Objective: Our aim was to extend our work in IL-13 biology to determine whether airway epithelial cell expression of 2 key mediators critical for SARS-CoV-2 infection, namely, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2), are modulated by IL-13. Methods: We determined effects of IL-13 treatment on ACE2 and TMPRSS2 expression ex vivo in primary airway epithelial cells from participants with and without type 2 asthma obtained by bronchoscopy. We also examined expression of ACE2 and TMPRSS2 in 2 data sets containing gene expression data from nasal and airway epithelial cells from children and adults with asthma and allergic rhinitis. Results: IL-13 significantly reduced ACE2 and increased TMPRSS2 expression ex vivo in airway epithelial cells. In 2 independent data sets, ACE2 expression was significantly reduced and TMPRSS2 expression was significantly increased in the nasal and airway epithelial cells in type 2 asthma and allergic rhinitis. ACE2 expression was significantly negatively associated with type 2 cytokines, whereas TMPRSS2 expression was significantly positively associated with type 2 cytokines. Conclusion: IL-13 modulates ACE2 and TMPRSS2 expression in airway epithelial cells in asthma and atopy. This deserves further study with regard to any effects that asthma and atopy may render in the setting of COVID-19 infection.
• Kimura, H., Francisco, D., Conway, M., Martinez, F. D., Vercelli, D., Polverino, F., Billheimer, D., & Kraft, M. (2020). Type 2 inflammation modulates ACE2 and TMPRSS2 in airway epithelial cells. The Journal of allergy and clinical immunology, 146(1), 80-88.e8.
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  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has dramatically changed our world, country, communities, and families. There is controversy regarding risk factors for severe COVID-19 disease. It has been suggested that asthma and allergy are not highly represented as comorbid conditions associated with COVID-19.
• Morin, A., McKennan, C. G., Pedersen, C. T., Stokholm, J., Chawes, B. L., Malby Schoos, A. M., Naughton, K. A., Thorsen, J., Mortensen, M. S., Vercelli, D., Trivedi, U., Sørensen, S. J., Bisgaard, H., Nicolae, D. L., Bønnelykke, K., & Ober, C. (2020). Epigenetic landscape links upper airway microbiota in infancy with allergic rhinitis at 6 years of age. The Journal of allergy and clinical immunology, 146(6), 1358-1366.
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  The upper airways present a barrier to inhaled allergens and microbes, which alter immune responses and subsequent risk for diseases, such as allergic rhinitis (AR).
• Pivniouk, V., Gimenes Junior, J. A., Honeker, L., & Vercelli, D. (2020). The Role of Innate Immunity in Asthma Development and Protection: Lessons from the Environment. Clinical and Experimental Allergy (Cover), 282-290, 50.
• Hrusch, C. L., Stein, M. M., Gozdz, J., Holbreich, M., von Mutius, E., Vercelli, D., Ober, C., & Sperling, A. I. (2019). T-cell phenotypes are associated with serum IgE levels in Amish and Hutterite children. The Journal of allergy and clinical immunology, 144(5), 1391-1401.e10.
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  Amish children raised on traditional farms have lower atopy and asthma risk than Hutterite children raised on modern farms. In our previous study we established that the Amish environment affects the innate immune response to decrease asthma and atopy risk. Here we investigated T-cell phenotypes in the same Amish and Hutterite children as in our earlier study to elucidate how this altered innate immunity affects adaptive T cells.
• Vercelli, D., & Bleecker, E. R. (2019). Strength in numbers: The quest for asthma genes. The Journal of Allergy and Clinical Immunology, 144(2), 413-415.
• DeVries, A., & Vercelli, D. (2018). Of pleiotropy and trajectories: Does the TGF-β pathway link childhood asthma and chronic obstructive pulmonary disease?. The Journal of Allergy and Clinical immunology, 141(6), 1992-1996.
• Rothers, J., Stern, D. A., Lohman, I. C., Spangenberg, A., Wright, A. L., DeVries, A., Vercelli, D., & Halonen, M. (2018). Maternal Cytokine Profiles during Pregnancy Predict Asthma in Children of Mothers without Asthma. American journal of respiratory cell and molecular biology, 59(5), 592-600.
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  Little is known about whether maternal immune status during pregnancy influences asthma development in the child. We measured cytokine production in supernatants from mitogen-stimulated peripheral blood immune cells collected during and after pregnancy from the mothers of children enrolled in the Tucson Infant Immune Study, a nonselected birth cohort. Physician-diagnosed active asthma in children through age 9 and a history of asthma in their mothers were assessed through questionnaires. Maternal production of each of the cytokines IL-13, IL-4, IL-5, IFN-γ, IL-10, and IL-17 during pregnancy was unrelated to childhood asthma. However, IFN-γ/IL-13 and IFN-γ/IL-4 ratios during pregnancy were associated with a decreased risk of childhood asthma (n = 381; odds ratio [OR], 0.33; 95% confidence interval [CI], 0.17-0.66; P = 0.002; and n = 368; OR, 0.36; 95% CI, 0.18-0.71; P = 0.003, respectively). The inverse relations of these two ratios with childhood asthma were only evident in mothers without asthma (n = 309; OR, 0.18; 95% CI, 0.08-0.42; P = 0.00007; and n = 299; OR, 0.17; 95% CI, 0.07-0.39; P = 0.00003, respectively) and not in mothers with asthma (n = 72 and 69, respectively; P for interaction by maternal asthma = 0.036 and 0.002, respectively). Paternal cytokine ratios were unrelated to childhood asthma. Maternal cytokine ratios in mothers without asthma were unrelated to the children's skin-test reactivity, total IgE, physician-confirmed allergic rhinitis at age 5, or eczema in infancy. To our knowledge, this study provides the first evidence that cytokine profiles in pregnant mothers without asthma relate to the risk for childhood asthma, but not allergy, and suggests a process of asthma development that begins in utero and is independent of allergy.
• Carr, T. F., Beamer, P. I., Rothers, J., Stern, D. A., Gerald, L. B., Rosales, C. B., Van Horne, Y. O., Pivniouk, O. N., Vercelli, D., Halonen, M., Gameros, M., Martinez, F. D., & Wright, A. L. (2017). Prevalence of Asthma in School Children on the Arizona-Sonora Border. The journal of allergy and clinical immunology. In practice, 5(1), 114-120.e2.
• DeVries, A., & Vercelli, D. (2017). The neonatal methylome as a gatekeeper in the trajectory to childhood asthma. Epigenomics, 9(4), 585-593.
• DeVries, A., Wlasiuk, G., Miller, S. J., Bosco, A., Stern, D. A., Lohman, I. C., Rothers, J., Jones, A. C., Nicodemus-Johnson, J., Vasquez, M. M., Curtin, J. A., Simpson, A., Custovic, A., Jackson, D. J., Gern, J. E., Lemanske, R. F., Guerra, S., Wright, A. L., Ober, C., , Halonen, M., et al. (2017). Epigenome-wide analysis links SMAD3 methylation at birth to asthma in children of asthmatic mothers. The Journal of allergy and clinical immunology, 140(2), 534-542.
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  The timing and mechanisms of asthma inception remain imprecisely defined. Although epigenetic mechanisms likely contribute to asthma pathogenesis, little is known about their role in asthma inception.
• Long, X., Daya, M., Zhao, J., Rafaels, N., Liang, H., Potee, J., Campbell, M., Zhang, B., Araujo, M. I., Oliveira, R. R., Mathias, R. A., Gao, L., Ruczinski, I., Georas, S. N., Vercelli, D., Beaty, T. H., Barnes, K. C., Chen, X., & Chen, Q. (2017). The role of ST2 and ST2 genetic variants in schistosomiasis. The Journal of allergy and clinical immunology, 140(5), 1416-1422.e6.
• Ober, C., Sperling, A. I., von Mutius, E., & Vercelli, D. (2017). Immune development and environment: lessons from Amish and Hutterite children. Current opinion in immunology, 48, 51-60.
• Vercelli, D. (2017). Are We What Our Mothers Made Us? Lessons from Epigenetics. The Journal of allergy and clinical immunology.
• Vercelli, D. (2017). When Innate Responses Matter: ILC2s Loom Large in Allergic Airway Inflammation. American Journal of Respiratory and Critical Care Medicine, 195(12), 1544-1546. doi:10.1164/rccm.201702-0299ed
• Vercelli, D. (2017). When Innate Responses Matter: ILC2s Loom Large in Allergic Airway Inflammation. American journal of respiratory and critical care medicine, 195(12), 1544-1546.
• DeVries, A., & Vercelli, D. (2016). Epigenetic Mechanisms in Asthma. Annals of the American Thoracic Society, 13 Suppl 1, S48-50.
• Gozdz, J., Holbreich, M., Metwali, N., Thorne, P. S., Sperling, A. I., Martinez, F. D., Ober, C., von Mutius, E., & Vercelli, D. (2016). Amish and Hutterite Environmental Farm Products Have Opposite Effects on Experimental Models of Asthma. Annals of the American Thoracic Society, 13 Suppl 1, S99.
• Gozdz, J., Ober, C., & Vercelli, D. (2016). Innate Immunity and Asthma Risk. The New England journal of medicine, 375(19), 1898-1899.
• Stein, M. M., Hrusch, C. L., Gozdz, J., Igartua, C., Pivniouk, V., Murray, S. E., Ledford, J. G., Marques dos Santos, M., Anderson, R. L., Metwali, N., Neilson, J. W., Maier, R. M., Gilbert, J. A., Holbreich, M., Thorne, P. S., Martinez, F. D., von Mutius, E., Vercelli, D., Ober, C., & Sperling, A. I. (2016). Innate Immunity and Asthma Risk in Amish and Hutterite Farm Children. The New England journal of medicine, 375(5), 411-21.
• Vercelli, D. (2016). A Virtuous Duplicity: 17q21 Variants at the Intersection between Asthma Protection and Risk. American journal of respiratory and critical care medicine, 193(8), 821-2.
• Vercelli, D. (2016). A virtuous duplicity: 17q21 variants at the intersection between asthma protection and risk. Editorial. Am. J. Respir. Crit. Care Med..
• Vercelli, D. (2016). Does epigenetics play a role in human asthma?. Allergol. Int., 65, 123-126.
• Vercelli, D., Mathias, R., Pivniouk, V. I., Rosenbaum, D., Herrell, A., Pivniouk, O., Rafaels, N., & Barnes, K. (2016). Differential regulation of human and mouse IL33 expression in the lungs of human IL33 BAC transgenic mice.. The Journal of Immunology, 196(1_Supplement), 120.2-120.2. doi:10.4049/jimmunol.196.supp.120.2
• Xu, H., Radabaugh, T., Lu, Z., Galligan, M., Billheimer, D., Vercelli, D., Wright, A. L., Monks, T. J., Halonen, M., & Lau, S. S. (2016). Exploration of Early-Life Candidate Biomarkers for Childhood Asthma Using Antibody Arrays. Pediatric Allergy and Immunology.
• DeVries, A., & Vercelli, D. (2015). Early predictors of asthma and allergy in children: the role of epigenetics. Curr. Opin. Allergy Clin. Immunol, 15(5), 435-9.
• DeVries, A., & Vercelli, D. (2015). Epigenetics in allergic diseases. Curr. Opin. Pediatr, 719-23.
• Long, X., Chen, Q., Zhao, J., Rafaels, N., Mathias, P., Liang, H., Potee, J., Campbell, M., Zhang, B., Gao, L., Georas, S. N., Vercelli, D., Beaty, T. H., Ruczinski, I., Mathias, R., Barnes, K. C., & Chen, X. (2015). An IL-13 promoter polymorphism associated with liver fibrosis in patients with Schistosoma japonicum. PloS one, 10(8), e0135360.
• Schaub, B., & Vercelli, D. (2015). Environmental protection from allergic diseases: From humans to mice and back. Curr. Opin. Immunol, 36, 88-93.
• Vercelli, D. (2015). The farm effect and allergic rhinitis. Global Atlas of Allergic Rhinitis and Chronic Rhinosinusitis, European Academy of Allergy and Clinical Immunology, 101-102.
• Vercelli, D., & Galli, S. J. (2015). Editorial overview: Allergy and hypersensitivity: New developments in allergy and type 2 immunity: never a dull moment. Curr. Opin. Immunol, 36, ix-xi.
• Vercelli, D., Gozdz, J., & von Mutius, E. (2014). Innate lymphoid cells in asthma: when innate immunity comes in a Th2 flavor. Current opinion in allergy and clinical immunology, 14(1), 29-34.
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  Asthma is typically considered as an immunologic Th2 cell-mediated disease, a notion that is still inspiring many therapeutic strategies. In the past years, however, an innate immune cell type has been discovered in mice that resides in the mucosa and secretes the Th2 cytokines IL-13 and IL-5 in response to IL-33 and IL-25 released by a damaged epithelium. These cells [now named group 2 innate lymphoid cells (ILC2s)] are rare, systemically dispersed, long-lived, and exist in humans. Recent work shows that ILC2s are critical for the development of asthma and related phenotypes in mice. Their role in human asthma remains unknown.
• Devries, A., & Vercelli, D. (2013). Epigenetics of human asthma and allergy: promises to keep. Asian Pacific journal of allergy and immunology, 31(3), 183-9.
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  The interest in asthma epigenetics is high because epigenetic mechanisms likely contribute to the environmental origins of the disease and its phenotypic variability. This review presents the main findings of asthma epigenetics and the challenges that still delay progress.
• Lau, S. S., Halonen, M., Vercelli, D., Xu, H., Radabaugh, T., Lu, Z., & Billheimer, D. (2013). Validation of an Early Life Candidate Biomarker for Childhood Asthma. The FASEB Journal, 27(S1). doi:10.1096/fasebj.27.1_supplement.1107.2
• Martinez, F. D., & Vercelli, D. (2013). Asthma. Lancet (London, England), 382(9901), 1360-72.
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  Asthma is a heterogeneous group of conditions that result in recurrent, reversible bronchial obstruction. Although the disease can start at any age, the first symptoms occur during childhood in most cases. Asthma has a strong genetic component, and genome-wide association studies have identified variations in several genes that slightly increase the risk of disease. Asthma is often associated with increased susceptibility to infection with rhinoviruses and with changes in the composition of microbial communities colonising the airways, but whether these changes are a cause or consequence of the disease is unknown. There is currently no proven prevention strategy; however, the finding that exposure to microbial products in early life, particularly in farming environments, seems to be protective against asthma offers hope that surrogates of such exposure could be used to prevent the disease. Genetic and immunological studies point to defective responses of lung resident cells, especially those associated with the mucosal epithelium, as crucial elements in the pathogenesis of asthma. Inhaled corticosteroids continue to be the mainstay for the treatment of mild and moderate asthma, but limited adherence to daily inhaled medication is a major obstacle to the success of such therapy. Severe asthma that is refractory to usual treatment continues to be a challenge, but new biological therapies, such as humanised antibodies against IgE, interleukin 5, and interleukin 13, offer hope to improve the quality of life and long-term prognosis of severe asthmatics with specific molecular phenotypes.
• Lau, S. S., Halonen, M., Vercelli, D., Xu, H., Radabaugh, T., Lu, Z., & Billheimer, D. (2012). Discovery of Early Life Plasma Protein Signatures for Asthma Development. The FASEB Journal, 26(S1). doi:10.1096/fasebj.26.1_supplement.1122.2
• Wlasiuk, G., & Vercelli, D. (2012). The farm effect, or: when, what and how a farming environment protects from asthma and allergic disease. Current opinion in allergy and clinical immunology, 12(5), 461-6.
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  Multiple studies have shown that the prevalence of asthma and atopy is reduced in children raised on traditional dairy farms. This article discusses the temporal constraints for the protective farm effect, the components of a farming environment that are associated with protection, and novel mechanisms that may underlie protection from asthma and atopy in farming populations.
• Mostecki, J., Cassel, S. L., Klimecki, W. T., Stern, D. A., Knisz, J., Iwashita, S., Graves, P., Miller, R. L., van Peer, M., Halonen, M., Martinez, F. D., Vercelli, D., & Rothman, P. B. (2011). A SOCS-1 promoter variant is associated with total serum IgE levels. Journal of immunology (Baltimore, Md. : 1950), 187(5), 2794-802.
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  SOCS-1 is a critical regulator of multiple signaling pathways, including those activated by cytokines that regulate Ig H chain class switching to IgE. Analysis of mice with mutations in the SOCS-1 gene demonstrated that IgE levels increase with loss of SOCS-1 alleles. This suggested that overall SOCS-1 acts as an inhibitor of IgE expression in vivo. A genetic association study was performed in 474 children enrolled in the Tucson Children's Respiratory Study to determine if genetic variation in the SOCS-1 locus correlates with altered levels of IgE. Carriers of the C-allele for a novel, 3' genomic single nucleotide polymorphism (SNP) in the SOCS-1 gene (SOCS1+1125G > C; rs33932899) were found to have significantly lower levels of serum IgE compared with those of homozygotes for the G-allele. Analysis demonstrated that the SOCS1+1125G > C SNP was in complete linkage disequilibrium with an SNP at position SOCS1-820G > T (rs33977706) of the SOCS-1 promoter. Carriers of the T-allele at the SOCS1-820G > T were also found to be associated with the decreased IgE. The promoter SNP increased transcriptional activity of the SOCS-1 promoter in reporter assays and human B cells. Consistent with this observation, the presence of this polymorphism within the promoter abolished binding of yin yang-1, which is identified as a negative regulator of SOCS-1 transcriptional activity. These data suggest that genetic variation in the SOCS-1 promoter may affect IgE production.
• Ober, C., & Vercelli, D. (2011). Gene-environment interactions in human disease: nuisance or opportunity?. Trends in genetics : TIG, 27(3), 107-15.
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  Many environmental risk factors for common, complex human diseases have been revealed by epidemiologic studies, but how genotypes at specific loci modulate individual responses to environmental risk factors is largely unknown. Gene-environment interactions will be missed in genome-wide association studies and could account for some of the 'missing heritability' for these diseases. In this review, we focus on asthma as a model disease for studying gene-environment interactions because of relatively large numbers of candidate gene-environment interactions with asthma risk in the literature. Identifying these interactions using genome-wide approaches poses formidable methodological problems, and elucidating molecular mechanisms for these interactions has been challenging. We suggest that studying gene-environment interactions in animal models, although more tractable, might not be sufficient to shed light on the genetic architecture of human diseases. Lastly, we propose avenues for future studies to find gene-environment interactions.
• Finkelman, F. D., Boyce, J. A., Vercelli, D., & Rothenberg, M. E. (2010). Key advances in mechanisms of asthma, allergy, and immunology in 2009. The Journal of allergy and clinical immunology, 125(2), 312-8.
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  The year 2009 was marked by rapid progress in understanding cellular and chemical mechanisms in the pathogenesis of asthma and other allergic disorders. Studies published in the Journal of Allergy and Clinical Immunology described advances in our knowledge of signaling molecules and pathways, cytokines, and activation and tolerance in asthma and murine models of this disease; food allergy; anaphylaxis and immediate hypersensitivity; mast cells and their disorders; atopic dermatitis; allergic conjunctivitis; nasal polyposis; and hypereosinophilic syndromes. Additional studies provided novel information about the induction and regulation of allergic inflammation and the genetic determinants of asthma and responsiveness to asthma therapy. Critical features of these studies and their potential effect on human atopic disorders are summarized here.
• Kiesler, P., Haynes, P. A., Shi, L., Kao, P. N., Wysocki, V. H., & Vercelli, D. (2010). NF45 and NF90 regulate HS4-dependent interleukin-13 transcription in T cells. Journal of Biological Chemistry, 285(Issue 11). doi:10.1074/jbc.m109.041004
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  Expression of the cytokine interleukin-13 (IL13) is critical for Th2 immune responses and Th2-mediated allergic diseases. Activation of human IL13 expression involves chromatin remodeling and formation of multiple DNase I-hypersensitive sites throughout the locus. Among these, HS4 is detected in the distal IL13 promoter in both naive and polarized CD4+ T cells. We show herein that HS4 acts as a position-independent, orientation-dependent positive regulator of IL13 proximal promoter activity in transiently transfected, activated human CD4+ Jurkat T cells and primary murine Th2 cells. The 3′-half of HS4 (HS4-3′) was responsible for IL13 up-regulation and bound nuclear factor (NF) 90 and NF45, as demonstrated by DNA affinity chromatography coupled with tandem mass spectrometry, chromatin immunoprecipitation, and gel shift analysis. Notably, the CTGTT NF45/NF90-binding motif within HS4-3′ was critical for HS4-dependent upregulation of IL13 expression. Moreover, transfection of HS4-IL13 reporter vectors into primary, in vitro differentiated Th2 cells from wild-type, NF45+/-, or NF90+/- mice showed that HS4 activity was exquisitely dependent on the levels of endogenous NF45 (and to a lesser degree NF90), because HS4-dependent IL13 expression was virtually abrogated in NF45+/- cells and reduced in NF90+/- cells. Collectively, our results identify NF45 and NF90 as novel regulators of HS4-dependent human IL13 transcription in response to T cell activation. © 2010 by The American Society for Biochemistry and Molecular Biology, Inc.
• Kiesler, P., Haynes, P. A., Shi, L., Kao, P. N., Wysocki, V. H., & Vercelli, D. (2010). NF45 and NF90 regulate HS4-dependent interleukin-13 transcription in T cells. The Journal of biological chemistry, 285(11), 8256-67.
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  Expression of the cytokine interleukin-13 (IL13) is critical for Th2 immune responses and Th2-mediated allergic diseases. Activation of human IL13 expression involves chromatin remodeling and formation of multiple DNase I-hypersensitive sites throughout the locus. Among these, HS4 is detected in the distal IL13 promoter in both naive and polarized CD4(+) T cells. We show herein that HS4 acts as a position-independent, orientation-dependent positive regulator of IL13 proximal promoter activity in transiently transfected, activated human CD4(+) Jurkat T cells and primary murine Th2 cells. The 3'-half of HS4 (HS4-3') was responsible for IL13 up-regulation and bound nuclear factor (NF) 90 and NF45, as demonstrated by DNA affinity chromatography coupled with tandem mass spectrometry, chromatin immunoprecipitation, and gel shift analysis. Notably, the CTGTT NF45/NF90-binding motif within HS4-3' was critical for HS4-dependent up-regulation of IL13 expression. Moreover, transfection of HS4-IL13 reporter vectors into primary, in vitro differentiated Th2 cells from wild-type, NF45(+/-), or NF90(+/-) mice showed that HS4 activity was exquisitely dependent on the levels of endogenous NF45 (and to a lesser degree NF90), because HS4-dependent IL13 expression was virtually abrogated in NF45(+/-) cells and reduced in NF90(+/-) cells. Collectively, our results identify NF45 and NF90 as novel regulators of HS4-dependent human IL13 transcription in response to T cell activation.
• Maier, R. M., Palmer, M. W., Andersen, G. L., Halonen, M. J., Josephson, K. C., Maier, R. S., Martinez, F. D., Neilson, J. W., Stern, D. A., Vercelli, D., & Wright, A. L. (2010). Environmental determinants of and impact on childhood asthma by the bacterial community in household dust. Applied and environmental microbiology, 76(8), 2663-7.
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  Asthma increased dramatically in the last decades of the 20th century and is representative of chronic diseases that have been linked to altered microbial exposure and immune responses. Here we evaluate the effects of environmental exposures typically associated with asthma protection or risk on the microbial community structure of household dust (dogs, cats, and day care). PCR-denaturing gradient gel analysis (PCR-DGGE) demonstrated that the bacterial community structure in house dust is significantly impacted by the presence of dogs or cats in the home (P = 0.0190 and 0.0029, respectively) and by whether or not children attend day care (P = 0.0037). In addition, significant differences in the dust bacterial community were associated with asthma outcomes in young children, including wheezing (P = 0.0103) and specific IgE (P = 0.0184). Our findings suggest that specific bacterial populations within the community are associated with either risk or protection from asthma.
• Strempel, J. M., Grenningloh, R., Ho, I., & Vercelli, D. (2010). Phylogenetic and functional analysis identifies Ets-1 as a novel regulator of the Th2 cytokine gene locus. Journal of immunology (Baltimore, Md. : 1950), 184(3), 1309-16.
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  The Th2 cytokine gene locus has emerged as a remarkable example of coordinated gene expression, the regulation of which seems to be rooted in an extensive array of cis-regulatory regions. Using a hypothesis-generating computational approach that integrated multispecies (n = 11) sequence comparisons with algorithm-based transcription factor binding-site predictions, we sought to identify evolutionarily conserved noncoding regions (ECRs) and motifs shared among them, which may underlie coregulation. Twenty-two transcription factor families were predicted to have binding sites in at least two Th2 ECRs. The ranking of these shared motifs according to their distribution and relative frequency pointed to a regulatory hierarchy among the transcription factor families. GATA sites were the most prevalent and widely distributed, consistent with the known role of GATA3 as a Th2 master switch. Unexpectedly, sites for ETS-domain proteins were also predicted within several Th2 ECRs and the majority of these sites were found to support Ets-1 binding in vitro and in vivo. Of note, the expression of all three Th2 cytokines (IL-5, -13, and -4) was significantly and selectively decreased in Th2 cells generated from Ets-1-deficient mice. Collectively, these data suggest that Ets-1 contributes to Th2 cytokine gene regulation by interacting with multiple cis-regulatory regions throughout the Th2 locus.
• Vercelli, D. (2010). Gene-environment interactions in asthma and allergy: the end of the beginning?. Current opinion in allergy and clinical immunology, 10(2), 145-8.
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  The pathogenesis of asthma and allergy typically involves not only distinct genetic and environmental factors, but also interactions between the two. Innate-immunity genes [particularly CD14, toll-like receptor (TLR)4 and TLR2, the critical mediators of responses to bacteria in the extracellular space] play a prominent role in gene-environment interactions relevant to asthma-related phenotypes because the interaction between microbial load and the innate-immune system is a critical determinant of both immune function and allergy/asthma susceptibility. This review presents recent findings illustrating the role of gene-environment interactions in asthma/allergy susceptibility.
• Vercelli, D. (2010). Genetics and biology of asthma 2010: La' ci darem la mano.... Journal of Allergy and Clinical Immunology, 125(Issue 2). doi:10.1016/j.jaci.2009.12.976
• Vercelli, D. (2010). Genetics and biology of asthma 2010: La' ci darem la mano... The Journal of allergy and clinical immunology, 125(2), 347-8.
• Vercelli, D., Pivniouk, V., Bailey, T., Pivniouk, O., Kiesler, P., Wlasiuk, G., Rosenbaum, D., Kim, K., Strempel, J., & Daines, M. (2010). Faithful epigenetic and transcriptional regulation of a transgenic human Th2 cytokine gene locus in the murine nuclear environment (51.1). The Journal of Immunology, 184(1_Supplement), 51.1-51.1. doi:10.4049/jimmunol.184.supp.51.1
• von Mutius, E., & Vercelli, D. (2010). Farm living: effects on childhood asthma and allergy. Nature reviews. Immunology, 10(12), 861-8.
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  Numerous epidemiological studies have shown that children who grow up on traditional farms are protected from asthma, hay fever and allergic sensitization. Early-life contact with livestock and their fodder, and consumption of unprocessed cow's milk have been identified as the most effective protective exposures. Studies of the immunobiology of farm living point to activation and modulation of innate and adaptive immune responses by intense microbial exposures and possibly xenogeneic signals delivered before or soon after birth.
• Kiesler, P., Shakya, A., Tantin, D., & Vercelli, D. (2009). An allergy-associated polymorphism in a novel regulatory element enhances IL13 expression. Human molecular genetics, 18(23), 4513-20.
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  IL-13 is a central effector of Th2-mediated allergic inflammation and is critical for the induction of IgE synthesis. Common IL13 variants are associated with allergy phenotypes in populations of distinct ethnic background. We recently demonstrated that IL13 expression by human CD4+ T cells is paralleled by extensive IL13 locus remodeling, which results in the appearance of multiple DNase I hypersensitive sites. Among these, HS4 in the distal promoter is constitutive in both naïve and polarized Th1 and Th2 cells, and spans a common single nucleotide polymorphism, IL13-1512A>C (rs1881457), strongly associated with total serum IgE levels. We recently characterized HS4 as a novel cis-acting element that upregulates IL13 transcription in activated human and murine T cells. Here we show that IL13-1512A>C is a functional polymorphism that significantly enhances HS4-dependent IL13 expression by creating a binding site for the transcription factor Oct-1. Of note, endogenous Oct-1 was preferentially recruited to the IL13-1512C risk allele in primary CD4+ T cells from IL13-1512A>C heterozygous subjects. Moreover, the IL13-1512C allele was overexpressed in transfected Th2 cells from Oct1(+/+) mice, but not from Oct1(+/-) mice, demonstrating that increased activity was exquisitely dependent on physiologic levels of Oct-1. Our results illustrate how a functional variant in a regulatory element enhances transcription of an allergy-associated gene, thereby modulating disease susceptibility.
• Vercelli, D. (2009). Of flaky tails and itchy skin. Nature genetics.
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  A new study defines the flaky tail mouse as a model for human atopic dermatitis caused by a null mutation in the gene encoding filaggrin, a key component of the epidermal barrier. Research in these mice will help explain how a disrupted barrier contributes to the pathogenesis of atopic dermatitis and to asthma arising in the context of atopic skin disease.
• Vercelli, D., Strempel, J. M., Grenningloh, R., & Ho, I. (2009). Phylogenetic and Functional Analysis Identifies Ets-1 as a Novel Regulator of the Th2 Cytokine Gene Locus. The Journal of Immunology, 184(3), 1309-1316. doi:10.4049/jimmunol.0804162
• Vercelli, D. (2008). Advances in asthma and allergy genetics in 2007. The Journal of allergy and clinical immunology, 122(2), 267-71.
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  This review discusses the main advances in the genetics of asthma and allergy published in the Journal in 2007. The association studies discussed herein addressed 3 main topics: the effect of the environment and gene-environment interactions on asthma/allergy susceptibility, the contribution of T(H)2 immunity gene variants to allergic inflammation, and the role of filaggrin mutations in atopic dermatitis and associated phenotypes. Other articles revealed novel, potentially important candidate genes or confirmed known ones. Collectively, the works published in 2007 reiterate that allergy and asthma are typical complex diseases; that is, they are disorders in which intricate interactions among environmental and genetic factors modify disease susceptibility by altering the fundamental structural and functional properties of target organs at critical developmental windows.
• Vercelli, D. (2008). Discovering susceptibility genes for asthma and allergy. Nature reviews. Immunology, 8(3), 169-82.
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  Asthma and asthma-related traits are complex diseases with strong genetic and environmental components. Rapid progress in asthma genetics has led to the identification of several candidate genes that are associated with asthma-related traits. Typically the phenotypic impact of each of these genes, including the ones most often replicated in association studies, is mild, but larger effects may occur when multiple variants synergize within a permissive environmental context. Despite the achievements made in asthma genetics formidable challenges remain. The development of novel, powerful tools for gene discovery, and a closer integration of genetics and biology, should help to overcome these challenges.
• Vercelli, D., Strempel, J. M., Grenningloh, R., & Ho, I. (2008). Phylogenetic and Functional Analyses Identify Ets‐1 as an Important Regulator of the Th2 Cytokine Gene Locus. The FASEB Journal, 22(S1). doi:10.1096/fasebj.22.1_supplement.850.7
• Vercelli, D., Wysocki, V., Kiesler, P., Haynes, P., Shi, L., & Kao, P. (2008). NF90 and NF45 Regulate Interleukin‐13 (IL13) Gene Transcription in Human T Cells. The FASEB Journal, 22(S1). doi:10.1096/fasebj.22.1_supplement.850.13
• Agresti, A., & Vercelli, D. (1998). Structure and expression of human γ4 germline immunoglobulin transcripts (GLT). FASEB Journal, 12(5).
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  IL-4 induces both IgE and IgG4 in human B cells. The coregulation of these isotypes with functionally distinct properties is likely to be mediated at the level of germline transcription. To define the mechanisms of ∈/γ4 coregulation, it is necessary to analyze and compare the structure and function of the ∈ and γ4 germline promoters. We therefore cloned γ4 GLT by RT-PCR using a forward primer upstream of the splice donor site used by γ1 and γ3 GLT, and a reverse primer in the γ4 hinge region. The 411 bp fragment thus amplified from cDNA of PBMC stimulated with IL-4+anti-CD40 mAb contained the 3′ end of the Iγ4 exon correctly spliced to the 5′ portion of Cγ4. Sequence analysis located the human Iγ4 exon about 1.5 kb upstream of the switch γ4 region. RT-PCR analysis using additional 5′ primers indicated that γ4 GLT initiate at least 420 bp from the Iγ4 splice donor site and are colinear with the genomic sequence. Primer extension analysis on polyA+ RNA purified from BL-2 cells treated with IL-4+anti-CD40 mAb led to the identification of several transcription start sites located 550-590 bp upstream of the Iγ4 splice donor site. Reporter assays showed that a 2,064 bp BamHI/NaeI fragment that contains Iγ4 at the 3′ end has promoter activity and drives an 8-fold increase in transcription following stimulation of BL-2 cells with IL-4+anti-CD40 mAb. The BamHI/NaeI fragment contains one putative Stat6 and at least three putative NF-κB binding sites upstream of the transcription start sites. We are investigating the role of these sites in the regulation of γ4 germline transcription.
• Yu, W., Soprana, E., Cosentino, G., Volta, M., Lichenstein, H., Viale, G., & Vercelli, D. (1998). Soluble CD141-152 confers responsiveness to both lipoarabinomannan and lipopolysaccharide in a novel HL-60 cell bioassay. Journal of Immunology, 161(8). doi:10.4049/jimmunol.161.5.2084
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  CD14 is a pattern recognition receptor involved in the interaction with multiple ligands, including LPS from Gram-negative bacteria and lipoarabinomannan (LAM) from mycobacteria. While the interactions between LPS and soluble CD14 (sCD14) have been analyzed in detail, LAM/CD14 interactions remain uncharacterized due to the lack of suitable functional assays. We describe herein a novel bioassay for the analysis of CD14/ligand interactions. CD14-negative myeloid HL-60 cells up-regulate endogenous CD14 gene expression when stimulated with LPS in the presence of recombinant soluble CD141-348. Using the HL-60 bioassay, we showed that sCD141- 348 confers responsiveness not only to LPS, but also to LAM. The response to LAM, but not that to LPS, was highly dependent on LPS binding protein (LBP). The N-terminal half of CD14 was sufficient to mediate HL-60 responses to LAM, since HL-60 cells responded with similar efficiency when stimulated with LAM and LBP in the presence of sCD141-348 or sCD141-152. Thus, the N-terminal 152 amino acids of CD14 contain the site(s) involved in the interaction with LAM and LBP, as well as the residues required for LAM- dependent CD14 signaling.
• Verani, A., Scarlatti, G., Comar, M., Tresoldi, E., Polo, S., Giacca, M., Lusso, P., Siccardi, A. G., & Vercelli, D. (1997). C-C chemokines released by lipopolysaccharide (LPS)-stimulated human macrophages suppress HIV-1 infection in both macrophages and T cells. Journal of Experimental Medicine, 185(Issue 5). doi:10.1084/jem.185.5.805
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  Human immunodeficiency virus-1 (HIV-1) expression in monocyte-derived macrophages (MDM) infected in vitro is known to be inhibited by lipopolysaccharide (LPS). However, the mechanisms are incompletely understood. We show here that HIV-1 suppression is mediated by soluble factors released by MDM stimulated with physiologically significant concentrations of LPS. LPS-conditioned supernatants from MDM inhibited HIV-1 replication in both MDM and T cells. Depletion of C-C chemokines (RANTES, MIP-1α, and MIP-1β) neutralized the ability of LPS-conditioned supernatants to inhibit HIV-1 replication in MDM. A combination of recombinant C-C chemokines blocked HIV-1 infection as effectively as LPS. Here, we report an inhibitory effect of C-C chemokines on HIV replication in primary macrophages. Our results raise the possibility that monocytes may play a dual role in HIV infection: while representing a reservoir for the virus, they may contribute to the containment of the infection by releasing factors that suppress HIV replication not only in monocytes but also in T lymphocytes.
• Cosentino, G., Soprana, E., Thienes, C., Siccardi, A., Viale, G., & Vercelli, D. (1995). IL-13 down-regulates CD14 expression and TNF-α secretion in normal human monocytes. Journal of Immunology, 155(6).
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  CD14, a glycosylphosphatidylinositol (GPI)-linked protein expressed on monocytes and neutrophils, regulates monocyte-lymphocyte interactions and serves as the LPS receptor. We showed previously that IL-4 down-regulates the expression of human CD14 by acting at the transcriptional level. We now investigate whether CD14 expression could also be regulated by IL-13, another member of the chromosome 5 cytokine gene family. IL-13 dose-dependently inhibited CD14 expression on human monocytes. By contrast, expression of CD23 and CD11b was enhanced strongly. Down-regulation of CD14 involved neither shedding nor activation of endogenous GPI anchor-cleaving enzymes. Indeed, soluble CD14 was not increased in the supernatants of IL-13-stimulated monocytes, and expression of CD55/DAF, another GPI-linked protein, was unaffected by IL-13. CD14 transcript levels were reduced sixfold in IL-13- treated monocytes. These results suggest that IL-13 down-regulates membrane CD14 by suppressing CD14 RNA expression. IL-13-dependent down-regulation of CD14 resulted in the inhibition of CD14-mediated events. Indeed, CD14- mediated release of TNF-α was inhibited markedly (~75%) in monocytes stimulated with LPS (100 ng/ml) after a 72-h preincubation with IL-13. However, IL-13 also directly inhibited monokine secretion, because it blocked PMA-induced, CD14-independent TNF-α release. Down-regulation of CD14 and TNF-α secretion may play a major role in the anti-inflammatory effects of IL-13 on LPS-stimulated monocytes.
• Soprana, E., Vigo, E., Verani, A., Blom, J., Siccardi, A., Vercelli, D., & Viale, G. (1994). Antiidiotypic antibodies mimic molecular and functional properties of human IL-1β in vitro and in vivo. Lymphokine and Cytokine Research, 13(5).
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  We obtained affinity-purified polyclonal anti-id antibodies against mAb MhC1 and BrhC3, which recognize amino acids 133-147 at the N-terminus of mature human IL-1β. mAb MhC1 and BrhC3 have been shown to inhibit binding of IL-1β to type I IL-1R, and to neutralize IL-1β bioactivity in a number of in vitro assays. We show that affinity-purified antibodies against the MhC1 and BrhC3 idiotypes specifically bind to type I IL-1β IL-1R and that this binding is inhibited by both IL-1β and IL-1ra; anti-id antibodies were also able to trigger IL-1R-dependent events, such as IL-8 secretion by human skin fibroblasts and pyrogenic effect after injection in mice. These anti-id antibodies, therefore, behave as structural and functional 'images' of IL- 1β, both in vivo and in vitro. These data indicate the idiotypic strategy as a powerful tool to study the fine specificity of receptor-ligand interactions. Moreover, this is, to our knowledge, the first report showing that the 'internal image' of a cytokine can be active in vivo.
• Vercelli, D., & Geha, R. (1991). Regulation of IgE synthesis in humans: A tale of two signals. The Journal of Allergy and Clinical Immunology, 88(3). doi:10.1016/0091-6749(91)90087-5
• Helm, B., Kebo, D., Vercelli, D., Glovsky, M. M., Gould, H., Ishizaka, K., Geha, R., & Ishizaka, T. (1989). Blocking of passive sensitization of human mast cells and basophil granulocytes with IgE antibodies by a recombinant human ε-chain fragment of 76 amino acids. Proceedings of the National Academy of Sciences of the United States of America, 86(Issue 23). doi:10.1073/pnas.86.23.9465
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  The recombinant peptide corresponding to residues 301-376 at the junction of constant regions 2 and 3 of the human IgE ε chain blocked the in vivo passive sensitization of human skin mast cells and in vitro sensitization of human basophil granulocytes with human IgE antibodies. An injection of the recombinant peptide or E myeloma protein into normal skin sites 1 hr before sensitization with an allergic serum blocked passive sensitization. In this system, ~ 10-fold higher molar concentration of the recombinant peptide than E myeloma protein was required for 50% inhibition of Prausnitz-Kustner reactions. When the mononuclear cells of two normal individuals were preincubated with the recombinant peptide or E myeloma protein for 15 min before passive sensitization with the same allergic serum and the cells were challenged with an optimal concentration of an antigen, ~ 11- to 13-fold higher concentration of the recombinant peptide than E myeloma protein was required for 50% inhibition of antigen-induced histamine release. Further studies with several recombinant peptides indicated that amino acid residues 363-376 in the Fc ε-chain fragment are not essential for binding of the peptide to Fc ε-chain receptor I.
• Helm, B., Marsh, P., Vercelli, D., Padlan, E., Gould, H., & Geha, R. (1988). The mast cell binding site on human immunoglobulin E. Gynecologic Oncology, 29(1). doi:10.1038/331180a0
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  Antibodies of the immunoglobulin E isotype sensitize mast cells and basophils for antigen-induced mediator release by binding through the Fc portion to a high-affinity receptor (FcεR1, K(a) = 109 M-1) on the cell surface causing the clinical manifestations of type I hypersensitivity. As the amino acid sequence of the human epsilon chain is now known, attempts have been made to map the FcεRi binding site on IgE to a fragment smaller than Fcε using proteolytic cleavage products, none of which proved to be active. Cleavage between the Cε2 and Cε3 domains released two inactive fragments, suggesting that the junction between these segments could be important in receptor binding. This region is protected against protease digestion in the rat IgE complex with the receptor of rat basophilic leukaemia cells. Here we report the mapping of the mast cell receptor binding site on human IgE to a sequence of 76 amino acids at the Cε2/Cε3 junction. Recombinant peptides containing this sequence inhibit passive sensitization of skin mast cells in vivo and sensitize mast cells to degranulation by anti-IgE in vitro almost as efficiently as a myeloma IgE. Fragments containing the separate domains are inactive. Additional sequences are required for rapid assembly of fragments into disulphide-linked dimers, suggesting that a single chain can form the active site. In a three-dimensional model of the human Fcε, the two identical segments are far apart. Each folds to generate a cleft between the Cε2 and Cε3 domains on the surface of the Fcε. The docking of IgE on to mast cells could take place within this cleft.
• Franco Del Prete, G., Vercelli, D., Tiri, A., Maggi, E., Rossi, O., Romagnani, S., & Ricci, M. (1987). Effect of in vitro irradiation and cell cycle-inhibitory drugs on the spontaneous human IgE synthesis in vitro. The Journal of Allergy and Clinical Immunology, 79(Issue 1). doi:10.1016/s0091-6749(87)80019-2
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  The in vitro effects of radiation, diterpine forskolin (FK), and hydrocortisone (HC) on the in vitro spontaneous IgE synthesis by peripheral blood B-lymphocytes from atopic patients were investigated. Without affecting cell viability, in vitro irradiation inhibited in a dose-dependent fashion de novo IgE synthesis in vitro by B cells from all patients examined with a mean 40% reduction of in vitro IgE product, after treatment with 100 rads. In contrast, the in vitro IgE production by the U266 myeloma cell line was unaffected, even by irradiation, with 1600 rads. The addition to B cell culures from atopic patients of FK consistently resulted in a dose-dependent inhibition of the spontaneous IgE production in vitro. The addition to cultures of 10-5 and 10-6 molar concentations, of HC was also usually inhibitory, whereas lower HC concentrations were uneffective or even enhanced the spontaneous in vitro IgE synthesis. When 10-6 molar concentrations, of both HC and FK were combined in culture, a summation inhibitory effect on the spontaneous IgE synthesis was observed. In contrast, neither FK nor HC had inhibitory effect on the in vitro spontaneous IgE synthesis by the U266 myeloma cell line. The spontaneous in vitro IgE synthesis by B cells from patients with Hodgkin's disease, demonstrating high levels of serum IgE, was strongly reduced or virtually abolished after patients underwent total nodal irradiation to prevent the spread of the disease. In addition, the in vitro spontaneous IgE synthesis by B cells from atopic patients was markedly decreased or abolished by in vivo administration of betamethasone. Taken together, these data indicate that in vitro spontaneous IgE-producing cells that circulate in the peripheral blood of atopic patients or patients with Hodgkin's disease represent a heterogeneous population of B cells, most of which require progression through the proliferative cell cycle before becoming cells actively secreting IgE in vitro. (J Allergy Clin Immunol 1987:79:69-77.). © 1987 The C. V. Mosby Company.
• Del Prete, G., Vercelli, D., Tiri, A., Maggi, E., Mariotti, S., Pinchera, A., Ricci, M., & Romagnani, S. (1986). In vivo activated cytotoxic T cells in the thyroid infiltrate of patients with Hashimoto's thyroiditis. Clinical and Experimental Immunology, 65(1).
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  High proportions of T8+ cells with inverted T4/T8 ratio were found in freshly isolated thyroid lymphocytes from patients with Hashimoto's thyroiditis. In addition, about one third of thyroid infiltrating cells expressed the TAC antigen, whereas in patient peripheral blood (PB) or normal lymphocytes from PB lymphoid organs the percentage of TAC-positive cells was consistently lower than 10%. Following negative selection with OKT4 or OKT8 monoclonal antibodies and complement, TAC+ T cells were enriched in the T8+ cell population. Thyroid infiltrating T cells from two patients underwent two different cloning procedures. In the first, single T cells were initially activated with phytohaemagglutinin (PHA) and interleukin 2 (IL-2), in the other with recombinant IL-2 (rIL-2) alone. The majority of T cell clones obtained by initial PHA-stimulation (55-65%) had the T8+ phenotype, but the frequency of T8+ clones obtained by stimulating T cells with rIL-2 alone was even higher (78 & 71%, respectively). The majority of T8+ clones elicited by PHA (35/37 & 36/38) and all the T8+ clones (36/36 & 22/22) obtained from thyroid infiltrates with initial stimulation by rIL-2 displayed cytolytic activity. Most of cytolytic T8+ clones obtained from thyroid infiltrates with both cloning procedures, displayed NK activity against human K562 and MOLT-4 target cells, but not against NK-resistant target, such as Raji cells. These data suggest that in Hashimoto's disease a considerable proportion of thyroid infiltrating T cells are in vivo activated T8+ cytolytic T cells with NK activity, which may be of importance in determining or maintaining the tissue damage of the target gland.
• Prete, G. F., Maggi, E., Mariotti, S., Tiri, A., Vercelli, D., Parronchi, P., Macchia, D., Pinchera, A., Ricci, M., & Romagnani, S. (1986). Cytolytic t lymphocytes with natural killer activity in thyroid infiltrate of patients with hashimoto’s thyroiditis: Analysis at clonal level. Journal of Clinical Endocrinology and Metabolism, 62(Issue 1). doi:10.1210/jcem-62-1-52
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  T Lymphocytes from thyroid infiltrates and peripheral blood (PB) of 3 patients with Hashimoto's thyroiditis (HT) were cloned using a microculture system previously shown to allow the clonal expansion of virtually all PB T lymphocytes from normal individuals. The phenotypic and functional features of a total number of 153 clones from thyroid infiltrates and 206 clones from PB were examined and compared with those of 272 clones derived from normal PB and spleens. The majority of clones derived from thyroid infiltrates of patients with HT had the cytotoxic/suppressor (T8+) phenotype, whereas the majority of clones from PB expressed the helper/inducer (T4+) phenotype. In addition, a consistent proportion (25%) of clones derived from PB of one patient had a phenotype (T3+T4−T8−) that was only occasionally found on clones obtained from PB or spleens of normal subjects. Most clones derived from both PB and thyroid infiltrates of the patients with HT had cytolytic activity, as assessed by a lectin-dependent cytolytic assay against the murine P815 tumor cell line. The high frequency of cytotoxic T cells in thyroid infiltrates was related to the increased proportion of T8+ cells, whereas enhanced percentages of cytotoxic cell precursors with T4+ and T3+T4−T8− phenotypes primarily accounted for the high frequency of cytolytic T cells in the PB of the same patients. Many cytolytic T cell clones derived from thyroid infiltrates also had natural killer activity against human K562 and MOLT-4 target cells. These data provide the first functional analysis of T lymphocytes infiltrating the thyroid gland in patients with HT and suggest that the high proportions of cytolytic T cell precursors found in both thyroid infiltrates and PB of these patients may be of importance in determining the tissue damage in thyroid autoimmune disease. © 1986 by The Endocrine Society.
• Romagnani, S., Giudizi, G. M., Maggi, E., Almerigogna, F., Biagiotti, R., Delprete, G., Mazzetti, M., Aiessi, A., Vercelli, D., & Ricci, M. (1985). Synergy of B cell growth factor and interleukin 2 in the proliferation of activated human B cells. European Journal of Immunology, 15(Issue 12). doi:10.1002/eji.1830151203
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  The activity of purified interleukin 2 (IL2), obtained by the recombinant DNA technology, on the proliferative response of human B cells stimulated with low concentrations of anti‐μ antibody was investigated. Recombinant IL2 was capable of augmenting the proliferative response of anti‐μ‐activated B cells and the T cell activation (Tac) antigen was expressed on a substantial proportion of normal B cells stimulated with anti‐μ antibody. However, crude supernatants from protein A‐stimulated peripheral blood mononuclear cells, which were found to possess both IL2 and B cell growth factor (BCGF) activities, maintained the ability to promote proliferation of anti‐μ‐ activated B cells after depletion of IL2. In addition, supernatants from some T cell clones, apparently free of IL2 activity, displayed strong BCGF activity in the costimulation assay with anti‐μ antibody. This BCGF activity was found in 25 kDa fractions by gel filtration and it was unaffected by addition to the cultures of anti‐Tac antibody, which consistently inhibited the B cell proliferative response promoted by recombinant IL2. The proliferative response of anti‐μ‐activated B cells to clonal, IL2‐free supernatants containing BCGF and recombinant IL2 present together from the beginning of culture was close to the sum of responses to the two stimulants, separately. In addition, the presence of clonal supernatant containing BCGF from the beginning of culture had a synergistic effect in the response of activated B cells to the subsequent addition of IL2, whereas the initial presence of IL2 had no such an effect on the reactivity of anti‐μ‐stimulated B cells to the late addition of clonal supernatant containing BCGF. The synergistic effect of BCGF in the IL2‐promoted B cell proliferation was probably the result of the recruitment of a greater number of IL2‐reactive B cells. In fact, the number of Tac‐positive cells was significantly higher in 36‐h cultures established in the presence of anti‐μ antibody plus clonal supernatant containing BCGF than in cultures stimulated with anti‐μ antibody alone. Taken together, these data indicate that anti‐μ antibody promotes the expression by normal human B cells of distinct receptors for IL2 and a BCGF distinct from IL2. They also suggest that BCGF can exert a synergistic effect in the IL2‐promoted proliferation of activated B cells. Copyright © 1985 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim
• Selli, C., Cozzolino, F., Carini, M., Lenzi, R., & Vercelli, D. (1984). Serum beta 2 microglobulin levels in patients with renal cell carcinoma. Urological Research, 12(Issue 5). doi:10.1007/bf00256152
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  Serum B2m concentrations were evaluated preoperatively in 40 patients with renal cell carcinoma and normal renal function, as assessed by serum creatinine
• Selli, C., Cozzolino, F., Vercelli, D., & Mincione, G. P. (1983). A, B, O (H) antigenic determinants in superficial transitional cell tumors of bladder. Urology, 21(Issue 2). doi:10.1016/0090-4295(83)90007-9
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  The initial tumors of 21 patients who earlier had presented with superficial noninvasive transitional cell carcinoma of the bladder and who subsequently underwent cystectomy for invasive disease were examined by the specific red cell adherence test. Eighteen of 21 initial tumors (85.7%) were antigen negative. The time from initial tumor resection ranged from twelve to 168 months (mean thirty-eight months). Loss of blood group antigens indicated enhanced biologic aggressiveness of tumors. However the interval to invasion is sufficiently variable as to preclude the use of this assay for timing of radical cystectomy. © 1983.
• Cozzolino, F., Vercelli, D., Castigli, E., Becucci, A., & Guglielmo, R. D. (1982). A New Case of γ‐Heavy Chain Disease: Clinical and Immunochemical Studies. Scandinavian Journal of Haematology, 28(Issue 2). doi:10.1111/j.1600-0609.1982.tb00507.x
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  The detection of a γ‐heavy chain disease protein in the serum and urine of a patient with a history of Hodgkin's disease in complete remission is reported. The protein has been characterized as a γ1 dimer, MW 66000, beginning at Asp 221 residue in the hinge region. No clinical or laboratory findings of malignancy have been observed in the patient since the abnormal protein was detected. The pathogenesis of this association, unreported to date, is discussed on the basis of previously administered high‐dose anti‐neoplastic treatments and of immunological impairment. © Munksgaard 1982
• Miliani, A., Anichini, P., di Guglielmo, R., Pellegrini, G., Firorelli, C., Cuccuini, A., Cozzolino, F., & Vercelli, D. (1982). Cytochemical studies of bone marrow plasma cells in monoclonal gammapathies. Nouvelle Revue Francaise d'Hematologie, 24(1).
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  Three plasma cell enzymatic reactions - ATPase, acid phosphatase (AP), α-naphthyl acetate esterase (α-NAE) - were tested in a large number of bone marrow samples from patients with multiple myeloma (MM), benign monoclonal gammapathy (BMG) - idiopathic (iBMG) and secondary (sBMG) - polyclonal hypergammaglobulinemia (PH), Waldenstrom's macroglobulinemia (WM) and from normoglobulinemic subjects (NS). The purpose of the present study was to evaluate the significance of these reactions in differential diagnosis of BMG and initial or atypical MM. For each reaction results were expressed as scores and normal limits were statistically established. Our findings in MM, HPO and NS are consistent with previous reports (similar enzymatic pattern in NS and PH; depressed ATPase acivity, raised AP and α-NAE activities in most MM cases). In the BMG class, ATPase activity was normal in about 40% of iBMG, while it was depressed in the other cases; most sBMG had diminished ATPase activity. AP patterns were normal for both BMG groups. α-NAE activity was normal in 50% of iBMG, while it was raised in the other cases. All the reactions were normal in WM. In a bayesian analysis of cytochemical patterns of NS and MM subjects ATPase showed the highest diagnostic significance, followed by α-NAE and AP ATPase, therefore, seems to be the most useful criterion for the diagnosis of initial MM; low ATPase score BMG patients should therefore be carefully followed-up.
• Torsellini, A., Becucci, A., Citi, S., Cozzolino, F., Guidi, G., Lombardi, V., Vercelli, D., & Veloci, M. (1982). Effects of pressure excursions on human platelets. In vitro studies on betathromboglobulin (β-TG) and platelet factor 4 (PF 4) release and on platelet sensitivity to ADP-aggregation. Haematologica, 67(6).
• Vercelli, D., Cozzolino, F., Becucci, A., & Di Guglielmo, R. (1982). β2-Microglobulin in monoclonal gammopathies. Nouvelle Revue Francaise d'Hematologie, 24(2).
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  Serum β2m concentrations were evaluated in 130 samples from 77 patients with monoclonal gammopathies (42 multiple myelomas, 35 benign monoclonal gammopathies). A highly significant correlation (P < 0.001) was found between serum β2m and cell mass; mean serum β2m levels were statistically different in the three myeloma stages (P values ranging from P < 0.05 to P < 0.001). When benign monoclonal gammopathies and multiple myelomas were globally compared, mean β2m concentrations were significantly different (P < 0.001), but multiple comparisons showed that no difference existed between benign monoclonal gammopathies and low cell mass (stage I) myelomas. Serum β2m determinations are therefore not clinically useful for the differential diagnosis of monoclonal gammopathies.
• Vercelli, D., Di Guglielmo, R., Guidi, G., Scolari, L., Buricchi, L., & Cozzolino, F. (1980). Bone marrow percentage of plasma cells in the staging of monoclonal gammopathies. Nouvelle Revue Francaise d'Hematologie, 22(2).
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  In the present study, the relationships between percentage of bone marrow plasma cells (BMP%), tumor cell mass, stage, and survival are statistically analyzed in a large number (90) of monoclonal gammopathies (MG). Though BMP% has not been included among the criteria for the staging of multiple myeloma, our results indicate that the above mentioned parameters correlate at highly significant degrees. BMP% is therefore proposed as a new useful parameter in the staging of MG.
• Di Guglielmo, R., Guidi, G., & Vercelli, D. (1979). Some clinical, cytomorphological and therapeutical aspects of plasmocytoma and related syndromes (author's transl). Haematologica, 64(Issue).
• Di Guglielmo, R., Vercelli, D., & Guidi, G. (1979). Clinical and quantitative staging and monitoring of multiple myeloma. Analysis of 145 clinical cases. Recenti Progressi in Medicina, 66(4).

Proceedings Publications

• DeVries, A., Kimura, H., Kimura, N., Molzahn, A., Pivniouk, V. I., Vercelli, D., & Kraft, M. (2025, February).

  SARS-CoV-2 Spike Protein is Sufficient to Induce Enhanced Pro-inflammatory Transcriptional Responses in Nasal Epithelial Cells from Atopic Asthmatics

  . In 2025 AAAAI / WAO Joint Congress, Vol. 155.
• Vercelli, D., Pivniouk, V. I., Holbreich, M., Anderson, D., Pivniouk, O., Michael, A., Ezeh, P., DeVries, A., & VanLinden, S. (2025, February).

  B Cells are Required for the Asthma-Protective Activity of Amish Farm Dust Extracts

  . In 2025 AAAAI / WAO Joint Congress, 155, AB290.
• Kraft, M., Vercelli, D., Pivniouk, V., Kimura, H., Francisco, D., Conway, M., & Molzahn, A. (2022). Type-2 Cytokine Mitigates Inflammatory Response to SARS-CoV-2. In American Thoracic Society.
• Vercelli, D., Nikolich-Zugich, J., Anderson, D., Churko, J., Conway, M., Michael, A., DeVries, A., Pivniouk, V., Pivniouk, O., Uhrlaub, J., Pivniouk, D., VanLinden, S., Hahn, S., Malone, S., Ezeh, P., & Kraft, M. (2022). The OM-85 Bacterial Lysate Inhibits SARS-CoV-2 Infection of Epithelial Cells by Downregulating SARS-CoV-2 Receptor Expression. In American Thoracic Society.
• Pivniouk, V. I., Vercelli, D., Pivniouk, V. I., Pivniouk, O., Pasquali, C., Michael, A. N., Jr, J. A., Gozdz, J., Gimenes, J. A., Ezeh, P., Devries, A., & Abidov, A. (2020). Intra-Nasal Administration of the OM-85 Bacterial Lysate Strongly Protects from Experimental Asthma by Targeting Multiple Innate and Adaptive Immune Processes. In A21. AIRWAY IMMUNOLOGY.
• Pivniouk, V. I., Rosenbaum, D., Aryanpur, P., Pivniouk, O., Stern, D., Halonen, M., & Vercelli, D. (2013, January). Asthma/allergy-associated single nucleotide polymorphisms (SNPs) in IL13 strongly dysregulate human IL4 expression and IgE production. In Keystone Symposium: Type 2 Immunity: Initiation, Maintenance, Homeostasis and Pathology.
• Stern, D., Eder, W., Tebow, G., Lohman, I. C., Soprana, E., Braun-Fahrländer, C., Riedler, J., Nowakk, D., Von Mutius, E., Halonen, M., Vercelli, D., Bufe, A., Carr, D., Grize, L., Herz, U., Holst, O., Lauener, R. P., Maisch, S., Renz, H., , Schierl, R., et al. (2004, February 25, 2003). Rethinking Th2 antibody responses and allergic sensitization. In Symposium on Anaphylaxis, Novartis Foundation, London, UK.
  More info

  Human Th2 cytokines (interleukins 4 and 13) induce co-expression of IgE and IgG4 through sequential switching. The regulation of IgG4 responses and the role of these responses in the pathogenesis of allergy have not been characterized. We are addressing these issues by comparing and contrasting the expression of allergen-specific IgE and IgG4 in a population of European children thoroughly defined for lifestyle, environmental exposures and allergic phenotypes. The current analysis focused exclusively on children from non-farming families (n=493) in order to avoid potential effects of exposure to microbial products abundant in farming environments. We found that allergens induce Th2-mediated IgG4 and/or IgE responses in the majority of the population. Approximately two-thirds of the children had allergen-specific IgG4 but not IgE, only a minority had both IgG4 and IgE, only a few were negative for both, and virtually none had only IgE. The prevalence of asthma and hay fever was dramatically higher in children with high IgG4 and IgE compared to children who only mounted IgG4 or low IgG4 and IgE responses. These results appear to recapitulate different stages of in vivo Th2-dependent sequential switching from IgG4 to IgE. These patterns of Th2-induced antibody responses may warrant a redefinition of the notion of allergen sensitization. Copyright © Novartis Foundation 2004.
• Vercelli, D. (1999). To E or not to E?. In Int. Arch. Allergy Immunol. 116: 1-4 (1998), 54.

Presentations

• Lynch, S., Vercelli, D., Carr, T. F., Martinez, F., Rosales, C. B., Billheimer, D. D., Rabe, B. A., Pivniouk, V. I., Banskar, S., Hahn, S., Ezeh, P., VanLinden, S. R., Anderson, D., Pivniouk, O., Michael, A. N., & DeVries, A. (2025, October).

  Fecal Products from 1 mo-old Infants at Increased Risk of Asthma Activate a Novel B Cell/Il17/Neutrophil Axis that Promotes Lung Inflammation

  . 34th Biennial Symposium of the Collegium Internationale Allergologicum. Dubrovnik, Croatia: Collegium Internationale Allergologicum.
• Vercelli, D. (2025).

  Airway Treatment with Amish Farm Dust Extracts Protects against Acute Airway Rhinovirus Infection and Induces Enduring Anti-Viral Immune Training

  . 34th Biennial Symposium, Collegium Internationale Allergologicum, Dubrovnik, Croatia, October 28.
• Vercelli, D. (2025).

  Distinct Functional Properties of Gut Microbial Products from Infants with Distinct Respiratory Symptom Scores: Results from the BEAMS cohort

  . Annual Meeting, Asthma and Airway Disease Cooperative Research Centers, NIAID, Rockville, MD, November 19.
• Vercelli, D. (2025).

  Farms, Microbes, and a World without Asthma

  . 47th Annual Founders Day Lecture, University of Arizona College of Medicine, Tucson, AZ, November 17.
• Vercelli, D. (2025).

  Heat and Health

  . French-American Innovation Days, France-Arizona Institute for Global Grand Challenges, University of Arizona, Tucson, AZ, November 13, 2025.
• Vercelli, D. (2025, February 28).

  Protective Bacterial Lysates to Reduce Wheezing and Asthma.

  . Asthma and Immunology/World Allergy Organization Joint Meeting, San Diego, CA, February 28. San Diego, CA: Asthma and Immunology/World Allergy Organization Joint Meeting.
• Vercelli, D. (2025, February 5, 2025).

  How Microbial Products Protect from Asthma and Allergies

  . Grand Rounds, Department of Medicine & Center for Human Immunobiology, Northwestern University, Chicago, IL, February 5. Northwestern University, Chicago, IL.
• Vercelli, D. (2025, October 16-19).

  Disrupted Barriers: Ways to Restore

  . 5th Global Allergy Forum, Allergy & Environment – Loss of Balance and Ways to Restore It. CK-Care Medicine Campus, Davos, Switzerland, October 16-19.
• Vercelli, D. (2025, September 18).

  How Microbe-Rich Environments Protect from Asthma

  . Basic Medical Sciences Seminar Series, Department of Basic Medical Sciences, University of Arizona College of Medicine, Phoenix, September 18. Phoenix, AZ.
• Pivniouk, V. I., Pivniouk, O., Uhrlaub, J. L., Molzahn, A., Kimura, H., Ledford, J., Kraft, M., Nikolich-Zugich, J. Z., & Vercelli, D. (2023).

  IL-13 protects epithelial cells from SARS-CoV-2 infection by inhibiting early ACE2-mediated events

  . Immunology2023, The AAI Annual Meeting. Washington, DC: AAI.
• Vercelli, D., Malone, S. P., Ezeh, P., Han, R., Banskar, S., VanLinden, S. R., Michael, A. N., Pivniouk, O., Hahn, S., & Pivniouk, V. I. (2023, October).

  Preventive but not Therapeutic Administration of a Bacterial Lysate Suppresses Experimental Allergic Asthma

  . 33rd Biennial Symposium of the Collegium Internationale Allergologicum. Montréal, Canada: Collegium Internationale Allergologicum.
• Vercelli, D. (2021). An Update from the University of Arizona: Airway Administration of OM-85 Blocks Experimental Asthma by Targeting Dendritic Cells and the Epithelium/IL-33/ILC2 Axis.. Expert Panel, OM Pharma, Geneva, Switzerland.
• Vercelli, D. (2021). Epithelial Barrier Function and Microbial Exposures in Asthma. Asthma and Airway Disease Cooperative Research Centers Virtual Conference, NIH/NIAIDNIH/NIAID.
• Vercelli, D. (2021). Microbiome and Allergic Disease. 24th Meeting of the Department of Allergology, University of Milan, Milan, Italy (virtual).
• Vercelli, D. (2021). The Hygiene Hypothesis in 2021 – and Beyond.. 5th Conference of the Chinese College of Allergy and Asthma (CCAA 2021) (virtual).
• Vercelli, D. (2021, February). The Hygiene Hypothesis: Where Do We Stand in 2021?. American Academy of Allergy, Asthma and Immunology Virtual Annual MeetingAmerican Academy of Allergy, Asthma and Immunology.
• Vercelli, D. (2021, January). The BEAMS Program Project. Southwest Environmental Health Science Center, University of Arizona.
• Vercelli, D. (2020, August). COVID-19 Research in the Vercelli Lab. Department of Cellular and Molecular Medicine, University of Arizona. The University of Arizona.
• Vercelli, D. (2020, February). Role of Gut Microbiota in Asthma Pathogenesis. Gut Group, The University of Arizona.
• Vercelli, D. (2020, February). Unlocking the Secrets of the Microbiome. The Eva M. Holtby Endowed Keynote Address. 2020 Living Healthy with Arthritis Conference, Arthritis Center. The University of Arizona.
• Vercelli, D. (2020, January). Disease and the Environment: How Growing up on a Farm Protects from Asthma. AZ-PRIDE Program, University of Arizona.
• Vercelli, D. (2020, November). Microbiota, Epigenetics and Trained Immunity in the Trajectory from Pregnancy to Childhood Asthma. Asthma and Airway Disease Research Center, University of Arizona.
• Vercelli, D. (2020, November). Role of Innate Immunity in Asthma. Keynote Address. DAM XXIII, 23rd Meeting of the Department of Allergology, University of Milan, Milan, Italy,.
• Vercelli, D. (2020, October). Allergies, Microbes and Epigenetics. Alpha Epsilon Delta Pre-Health, The University of Arizona.
• Vercelli, D. (2020, October). La' ci darem la mano: Environmental and gut microbiomes converge to promote health or disease. NYC Urban Soils Institute, 5th Annual Symposium, Keynote Address.
• Honeker, L. K., Sharma, A., Gozdz, J., Theriault, B., Patil, K., Gimenes, Jr, J. A., Horner, A. N., Pivniouk, V. I., Igartua, C., Stein, M. M., Holbreich, M., von Mutius, E., Ober, C., Gilbert, J. A., & Vercelli, D. (2019, May 17-22). Gut microbiota from Amish but not Hutterite pre-school children protect germ-free mice from experimental asthma. International Conference, American Thoracic Society. Dallas, TX.
• Vercelli, D. (2019, February 13). Learning from the Environment How to Prevent Asthma. Research Day, University of Arizona. Tucson, AZ.
• Vercelli, D. (2019, February 23). Not All Eosinophils Are Created Equal. The 2019 Rebecca Buckley Lecture.. Annual Meeting, American Academy of Allergy, Asthma and Immunology. San Francisco, CA.
• Vercelli, D. (2019, January 21, 2019). Can Microbes Protect from Asthma? Studies with Amish and Hutterite Gut Microbiota.. Annual Meeting, Western Society of Allergy, Asthma and Immunology. Maui, HI.
• Vercelli, D. (2019, January 23). Epigenetics of Asthma: Can We Predict Childhood Disease at Birth or Even Earlier?. Annual Meeting, Western Society of Allergy, Asthma and Immunology. Maui, HI.
• Vercelli, D. (2019, July 10). Microbiota and Asthma. FASEB Science Research Conference, IgE and Allergy: From Mechanisms to Therapy. Scottsdale, AZ.
• Vercelli, D. (2019, June 18). Intra-nasal administration of OM-85 abrogates experimental allergic asthma. VIFOR/ Istituto per la Ricerca Biologica meeting. Bellizona, Switzerland.
• Vercelli, D. (2019, June 19). Microbiota and Asthma Protection. Istituto per la Ricerca Biologica. Bellizona, Switzerland.
• Vercelli, D. (2019, June 6). Gut Microbiota and Asthma Protection: Lessons from Gnotobiotic Mice.. Division of Immunology, Children’s Hospital/Harvard Medical School. Boston, MA.
• Vercelli, D. (2019, March 18). OM-85 Studies at the University of Arizona. VIFOR OM-Pharma. Geneva, Switzerland.
• Vercelli, D. (2019, November 13). Environmental Mechanisms of Asthma Protection. Department of Environmental Health, Harvard School of Public Health. Boston, MA.
• Vercelli, D. (2019, October 18). The Impact of Different Lifestyle Conditions on Asthma and Allergy Development. EAACI Pediatric Asthma and Allergy Meeting (PAAM). Florence, Italy.
• Vercelli, D. (2019, October 9). The Immunology of IgE. Novartis Preceptorship, Asthma and Airway Disease Research Center, University of Arizona. Tucson, AZ.
• Vercelli, D. (2019, September 24). Leveraging Gut Microbiota for Asthma Protection. Grand Rounds, Department of Internal Medicine, University of Oklahoma. Oklahoma City, OK.
• Vercelli, D. (2018, August 21). Understanding IL-4/IL-13 Function. Invited talk, Sanofi Preceptorship - Asthma and Airway Disease Research Center, University of Arizona. Tucson, AZ.
• Vercelli, D. (2018, July 23). How Exposure to an Amish Environment Affects Immune Responses and Asthma Pathogenesis. State-of-the-Art Speaker, 36th Aspen Allergy Conference. Aspen, CO.
• Vercelli, D. (2018, June 1). Understanding Asthma Protection and Risk: Studies in Gnotobiotic Mice. Copenhagen Prospective Studies on Asthma in Childhood Collaborative Symposium, “Prenatal Origins of Asthma”. Copenhagen, Denmark.
• Vercelli, D. (2018, June 25). OM-85 Studies at the University of Arizona. VIFOR OM-Pharma. Geneva, Switzerland.
• Vercelli, D. (2018, March 2). From Mom to Baby: Epigenetics and the Risk for Childhood Asthma. Invited Lecture, American Academy of Allergy, Asthma and Immunology/World Allergy Organization Joint Congress. Orlando, FL.
• Vercelli, D. (2018, March 2). The Microbiome: A Target for Atopy (and Asthma) Prevention. Invited Lecture, American Academy of Allergy, Asthma and Immunology/World Allergy Organization Joint Congress. Orlando, FL.
• Vercelli, D. (2018, May 28). Influencing Innate Immunity: Ways to Make It Work. Plenary Session, European Academy of Allergy and Clinical Immunology Congress 2018. Munich, Germany.
• Vercelli, D. (2018, May 5). The Molecular Genomics Landscape at the Asthma and Airway Disease Research Center. Asthma and Airway Disease Research Center Annual Retreat. Tucson, AZ.
• Vercelli, D. (2018, November 13). Are We What Our Mothers Made Us? Epigenetics Trajectories to Childhood Asthma. Invited talk, Transgenerational Epigenetics in Allergy Workshop, National Institute of Allergy and Infectious Diseases. Rockville, MD.
• Vercelli, D. (2018, October 1). Transplant of Amish but not Hutterite Gut Microbiota is Sufficient to Protect Germ-Free Mice from Experimental Asthma. Invited talk, 32nd Symposium, Collegium Internationale Allergologicum. Palma de Mallorca, Spain.
• Vercelli, D. (2018, October 17). Epigenetics Trajectories to Childhood Asthma: Are We What Our Mothers Made Us?. Genetics and Genomics Grand Rounds, Center for Applied Genetics and Genomic Medicine, University of Arizona. Tucson, AZ.
• Vercelli, D. (2018, October 19). Leveraging Epigenetic Data to Understand the Asthma Trajectory. Invited talk, Severe Asthma 2018: Advances in Pathogenesis and Treatment, Yale School of Medicine & Yale Center for Asthma and Airway Diseases, Yale University. New Haven, CT.
• Vercelli, D. (2017, April). Environmental Modulation of Allergic Inflammation: The Amish Paradigm. Keynote Address, 30th National Meeting, Italian Society of Allergology, Asthma and Clinical Immunology (SIAAIC).
• Vercelli, D. (2017, April). Epigenetics and the Human Asthma/COPD Continuum: A Tale of Trajectories. Presidential Symposium, International Conference, American Thoracic Society.
• Vercelli, D. (2017, April). Innate Immunity and Asthma Risk in Amish and Hutterite Farm Children. Selected CR Forum Top Ten Clinical Research Achievement Awardee Presentation, Translational Science 2017.
• Vercelli, D. (2017, December). Environmental Protection from Allergic Diseases: Lessons from Gnotobiotic Mice. Allergy and Pulmonology Research Group, Ludwig-Maximilian University, Munich, Germany.
• Vercelli, D. (2017, December). Regulatory Properties of OM-85: Present Evidence and Future Perspectives. Experts Workshop on Immunomodulation with OM-85, Rome.
• Vercelli, D. (2017, January). What the Neonatal Methylome Tells Us about the Trajectory to Childhood Asthma. Biweekly Research Conference, The Asthma and Airway Disease Research CenterUniversity of Arizona.
• Vercelli, D. (2017, June). Early Life Candidate Biomarkers in Childhood Asthma. Invited Lecture, World Allergy Organization/Japanese Society of Allergology Symposium, The 66th Annual Meeting of the Japanese Society of Allergology.
• Vercelli, D. (2017, March). Translating Asthma: From Genotype to Phenotype to Endotype. Annual Meeting, American Academy of Allergy, Asthma and Immunology.
• Vercelli, D. (2017, November). Environmental Protection from Allergic Diseases: From Humans to Mice and Back. 26th Johns Hopkins Asthma and Allergy Center Fall Symposium, Johns Hopkins Asthma and Allergy Center, Johns Hopkins University School of Medicine.
• Vercelli, D. (2017, November). Epigenetics of Asthma and Allergic Disease. DAM XX, 20th Meeting of the Department of Allergology, University of Milan, Milan, Italy.
• Vercelli, D. (2017, November). How the Environment Protects from Asthma: Studies in Gnotobiotic Mice. Asthma and Airway Disease Research Center Retreat, University of Arizona.
• Vercelli, D. (2017, November). How the Environment Protects from Asthma: Studies in Gnotobiotic Mice. Short Seminar, Department of Cellular and Molecular Medicine, University of Arizona.
• Vercelli, D. (2017, October). How the Environment Protects from Asthma and Allergy. Allergy and Immunology Division, Northwestern University.
• Vercelli, D. (2017, October). Learning from the environment how to prevent asthma. 50th Anniversary Innovations and Inventions Research Fair, College of Medicine, University of Arizona.
• Vercelli, D. (2017, October). OM-85 Studies at the University of Arizona. VIFOR-OM Pharma. Zurich.
• Vercelli, D. (2017, October). We are (fortunately) not alone: The microbiome, immunity and health – A personal account. The University of Arizona Osher Life-Long Learning Institute (OLLI).
• Vercelli, D. (2016, April). Environmental Protection from Asthma and Allergy: From Humans to Mice and Back. 31st Symposium, Collegium Internationale Allergologicum, Charleston, SC.
• Vercelli, D. (2016, April). How the Genome, the Epigenome and the Environment Shape the Trajectory to Childhood Asthma. Inaugural Symposium, The Center for Applied Genetics and Genomic MedicineThe University of Arizona.
• Vercelli, D. (2016, July). How the Environment Protects from Allergy and Asthma: From Humans to Mice and Back. FASEB Science Research Conference, “IgE and Allergy: 50 Years and Onward”, West Palm Beach, FL.
• Vercelli, D. (2016, March). A Colloquium on Language and Genetics: A conversation with Noam Chomsky. Workshop, The University of Arizona.
• Vercelli, D. (2016, March). Epigenetics in Asthma. 2016 Annual Meeting, American Academy of Allergy, Asthma and Immunology.
• Vercelli, D. (2016, March). How the environment protects from allergic inflammation. 18th Meakins-Christie Laboratory Symposium: "Asthma and COPD", Montreal, Canada.
• Vercelli, D. (2016, March). How the environment protects from allergic inflammation. Frontiers in Immunobiology & Immunopathogenesis SymposiumUniversity of Arizona, Tucson, AZ.
• Vercelli, D. (2016, October). Epigenetic Mechanisms of Asthma Inception. The Philip Fireman Lecture. The 11th International Nemacolin Asthma Conference, Nemacolin, PA.
• Vercelli, D. (2016, September). An Epigenetic Trajectory from Birth to Childhood Asthma. Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) Collaborative Symposium, “Prenatal Origins of Asthma”, Copenhagen, Denmark.
• Vercelli, D. (2015, April). Environmental Mechanisms of Allergy Protection: Studies in Humans and Mice. Department of Allergy and Clinical Immunology, University of Florence, Florence, Italy. Florence, Italy: Department of Allergy and Clinical Immunology, University of Florence, Florence, Italy.
• Vercelli, D. (2015, April). When and How the Environment Protects from Asthma: Studies in Humans and Mice. NIEHS Center Directors Meeting, University of Arizona, Tucson, AZ. University of Arizona: University of Arizona.
• Vercelli, D. (2015, June). Epigenetic Mechanisms in Asthma - The Gilles Filley Lecture. Thomas L. Petty Aspen Lung Conference, 58th Annual Meeting, Aspen, CO. Aspen, CO: University of Colorado.
• Vercelli, D. (2015, June). How The Environment and Its Microbes Protect From Asthma And Allergy: Studies in US Farming Population. Human Microbiome and Disease, Milan, Italy. Milan, Italy: University of Milan, Milan, italy.
• Vercelli, D. (2015, June). How the Environment Protects from Allergic Lung Inflammation. Istituto Nazionale di Genetica Molecolare Romeo ed Enrica Invernizzi, University of Milan, Milan, Itay. Istituto Nazionale di Genetica Molecolare Romeo ed Enrica Invernizzi: University of Milan, Milan, italy.
• Vercelli, D. (2015, June). Neonatal Epigenetic Predictors of Childhood Asthma. Society for In Vitro Biology, Annual Meeting, Tucson, AZ. Tucson, AZ: Society for In Vitro Biology.
• Vercelli, D. (2015, June). Sensing the Environment. European Academy of Allergy and Clinical Immunology Congress, Barcelona, Spain. Barcelona, Spain: European Academy of Allergy and Clinical Immunology.
• Vercelli, D. (2017, June). The Pathogenesis of Childhood Asthma: Lessons from the Environment. Invited Lecture, The 66th Annual Meeting of the Japanese Society of Allergology. Tokyo.

Poster Presentations

• Vercelli, D., Banskar, S., Michael, A. N., VanLinden, S. R., Pivniouk, O., Ezeh, P., Hahn, S., DeVries, A., & Pivniouk, V. I. (2025, October).

  Rapid Induction of Type-I Interferons by the OM-85 Bacterial Lysate Reduces Alternaria-Dependent Eosinophil Recruitment to the Airways

  . 34th Biennial Symposium of the Collegium Internationale Allergologicum. Dubrovnik, Croatia: Collegium Internationale Allergologicum.
• Vercelli, D., Chu, H. W., Kraft, M., Ezeh, P., Michael, A. N., Pivniouk, O., Banskar, S., Nouri, H., Hahn, S., DeVries, A., & Pivniouk, V. I. (2025, November).

  STRONG AND LONG-LASTING PROTECTION FROM VIRAL INFECTIONS BY AIRWAY ADMINISTRATION OF AMISH FARM DUST EXTRACTS 

  . Asthma and Allergic Diseases Cooperative Research Centers (AADCRC) Annual Steering Committee Meeting. Rockville, MD: National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH).
• DeVries, A. A., Michael, A., Pivniouk, O., Anderson, D., VanLinden, S., Ezeh, P., Hahn, S., Banskar, S., Pivniouk, V. I., & Vercelli, D. (2024). PHENOTYPIC AND TRANSCRIPTIONAL ANALYSES IN A MOUSE MODEL OF ASTHMA IDENTIFY BOTH PROTECTIVE AND NON-PROTECTIVE STERILE FECAL WATER (SFW) SAMPLES FROM 1 MONTH-OLD BEAMS PARTICIPANTS. 2024 Asthma and Allergic Diseases Cooperative Research Centers Annual Meeting.
• DeVries, A., Kimura, H., Kimura, N., Molzahn, A., Pivniouk, V. I., Vercelli, D., & Kraft, M. (2024). BINDING OF SARS-COV-2 SPIKE PROTEIN TO NASAL EPITHELIAL CELLS IS SUFFICIENT TO INDUCE AN ACUTE TRANSCRIPTIONAL PRO-INFLAMMATORY RESPONSE. 2024 Asthma and Allergic Diseases Cooperative Research Centers Annual Meeting.
• Vercelli, D., Kraft, M., Chu, H. W., Ledford, J., Ezeh, P., Pivniouk, O., Banskar, S., & Pivniouk, V. I. (2023). INTRANASAL ADMINISTRATION OF AMISH FARM DUST EXTRACTS PREVENTS RV1B-INDUCED LUNG NEUTROPHILIA. 2023 Asthma and Allergic Diseases Cooperative Research Centers Annual Meeting. Rockville, MD: NIAID.
• Vercelli, D., Pasquali, C., DeVries, A., Gozdz, J., Abidov, A., Pivniouk, O., Michael, A. N., Ezeh, P., Gimenes, Jr, J. A., & Pivniouk, V. I. (2020, May 15-20). Intra-nasal administration of the OM-85 bacterial lysate strongly protects from experimental asthma by targeting multiple innate and adaptive immune processes. International Conference, American Thoracic Society. Philadelphia, PA.
• Morin, A., McKennan, C., Thorsen, J., Stokholm, J., Chawes, B., Schoos, A., Naughton, K., Pedersen, C., Vercelli, D., Nicolae, D., Bonnelykke, K., Bisgaard, H., & Ober, C. (2019, October 15-19). Upper airway microbiota diversity in infancy is associated with nasal mucosa DNA methylation patterns and allergic rhinitis at 6 years of age. American Society of Human Genetics 2019 Annual Meeting. Houston, TX.
• Roth-Walter, F., al., e., Vercelli, D., von Mutius, E., & Jensen-Jarolim, E. (2019, June 1-6). Beta-lactoglobulin (BLG) accumulates in stable dust associated with zinc: potential implications for the allergy- and asthma-protective effect. European Academy of Allergy and Clinical Immunology 2019 Annual Meeting. Lisbon, Portugal.
• A., M., C., M., K., N., D., N., Vercelli, D., K., B., H., B., & C., O. (2018, October 16-20). DNA methylation in nasal epithelial cells and sensitization to aeroallergens. Annual Meeting, American Society for Human Genetics. San Diego, CA.
• Roth-Walter, F., al., e., Vercelli, D., von Mutius, E., & Jensen-Jarolim, E. (2018, December 6-9). Beta-lactoglobulin is present in cow stable dust and with its ligands prevent allergic sensitization and symptoms in mice. Implications for the allergy protective farm effect?. World Allergy Organization International Scientific Conference. Florence, Italy.
• DeVries, A., Stern, D., Wright, A. L., Halonen, M., & Vercelli, D. (2017, May). Neonatal DNA methylation profiles are associated with the maternal prenatal immune milieu selectively in children with non-asthmatic mothers.. International Conference, American Thoracic Society. Washington, DC.
• Pali-Schoell, I., Roth Walter, F., Hofstetter, G., Hann, S., Ahlers, S., Moussa-Afify, S., Wittek, T., Vercelli, D., von Mutius, E., & Jensen-Jarolim, E. (2017, June). The lipocalin beta-lactoglobulin (BLG) accumulates in stable dust: potential implications for the allergy- and asthma-protective effect.. European Academy of Allergy and Clinical Immunology 2017.
• Pali-Schoell, I., Roth Walter, F., Hofstetter, G., Hann, S., Ahlers, S., Moussa-Afify, S., Wittek, T., Vercelli, D., von Mutius, E., & Jensen-Jarolim, E. (2017, November). Identification of the cows’ milk protein beta-lactoglobulin in stable dust: potential implications for the allergy- and asthma-protective effect. Annual Meeting, Austrian Society of Allergology and Immunology.
• Carr, T. F., Beamer, P. I., Rothers, J., Stern, D. A., Gerald, L. B., Rosales, C. B., Van Horne, Y. O., Pivniouk, O. N., Vercelli, D., Halonen, M., Gameros, M., Martinez, F. D., & Wright, A. L. (2016, May). Prevalence of asthma in adolescents across the Arizona-Sonora border using ISAAC written and video questionnaires. International Conference, American Thoracic Society, San Francisco, CA.
• DeVries, A., Wlasiuk, G., Miller, S., Bosco, A., Stern, D., Lohman, I. C., Rothers, J. L., Jones, A., Nicodemus-Johnson, J., Curtin, J., Simpson, A., Custovic, A., Jackson, D., Gern, J., Lemanske, R., Guerra, S., Wright, A. L., Ober, C., Halonen, M., & Vercelli, D. (2016, Spring). Neonatal SMAD3 promoter hypermethylation predicts asthma in children of asthmatic mothers from three birth cohorts. International Conference, American Thoracic Society, San Francisco, CA.
• Hrsuch, C., Stein, M., Gozdz, J., Holbreich, M., von Mutius, E., Vercelli, D., Ober, C., & Sperling, A. (2016, November). Monocyte and Treg phenotypes in two U.S. farming populations mirror differential asthma and atopy risk: Studies in Amish and Hutterite children. Autumn Immunology Conference, Chicago, IL.
• Pivniouk, V. I., Rosenbaum, D., Herrell, A., Pivniouk, O., Rafaels, N., Mathias, R., Barnes, K., & Vercelli, D. (2016, May). Differential regulation of human and mouse IL33 expression in the lungs of human IL33 BAC transgenic mice.. AAI Annual Meeting - Immunology 2016.
• Pivniouk, V. I., Rosenbaum, D., Pivniouk, O., & Vercelli, D. (2016, May). Downregulation of human IL4 and IL13 expression by CRISPR/Cas9-mediated deletion of DNase I hypersensitive site HS11/12 from a transgenic human Th2 cytokine locus. AAI Annual Meeting - Immunology 2016.
• DeVries, A., Wlasiuk, G., Miller, S., Bosco, A., Stern, D., Nicodemus-Johnson, J., Jones, A., Rothers, J. L., Lohman, I. C., Wright, A. L., Ober, C., Halonen, M., & Vercelli, D. (2015, Spring). Neonatal epigenetic predictors of childhood asthma map to immunoregulatory and pro-inflammatory pathways. International Conference, American Thoracic Society.
• Gozdz, J., Holbreich, M., Metwali, N., Thorne, P., Sperling, A., Martinez, F., Ober, C., von Mutius, E., & Vercelli, D. (2015, Spring). Opposite effects of farming on asthma: mice exposed to Amish and Hutterite environmental products recapitulate asthma protection and risk. International Conference, American Thoracic Society. Denver, CO: American Thoracic Society.
• Hrusch, C., Stein, M., Igartua, C., Holbreich, M., Thorne, P., Vercelli, D., von Mutius, E., Ober, C., & Sperling, A. (2015, May). Differences in immune regulatory phenotypes in two U.S. farming populations mirror differential asthma and atopy risk: Studies in Amish and Hutterite school children. International Conference, American Thoracic Society. Denver, CO: American Thoracic Society.
• Kranch, R., Stern, D., Wright, A. L., Lohman, I. C., Spangenberg, A., Vercelli, D., Winzerling, J. J., Wilhelm, M. S., & Halonen, M. (2015, Spring). Temporal patterns of early life food-specific IgE and their relation to asthma, eczema, and allergic rhinitis at age 5. Frontiers in Immunobiology & Immunopathogenesis Symposium. University of Arizona.
• Stein, M., Hrusch, C., Igartua, C., Anderson, R., Metwali, N., Holbreich, M., Thorne, P., von Mutius, E., Vercelli, D., Sperling, A., & Ober, C. (2015, October). Dissecting genetic and environmental contributors to asthma and allergy in two founder populations. American Society for Human Genetics 2015 Annual Meeting. Baltimore, MD: American Society for Human Genetics.

Reviews

• Pivniouk, V. I., & Vercelli, D. (2023. The om-85 bacterial lysate: a new tool against sars-cov-2?. Multidisciplinary Respiratory Medicine.
• Vercelli, D., & Pivniouk, V. I. (2023. The om-85 bacterial lysate: a new tool against sars-cov-2?. Multidisciplinary Respiratory Medicine.

Others

• Vercelli, D. (2009). Gene-environment interactions: the road less traveled by in asthma genetics. The Journal of allergy and clinical immunology.