- Professor, Cellular and Molecular Medicine
- Professor, BIO5 Institute
- Associate Director, Asthma / Airway Disease Research Center
- Director, Arizona Center for the Biology of Complex Diseases (ABCD)
- Professor, Genetics - GIDP
Dr. Vercelli received her MD degree from the University of Florence in 1978 and trained in immunology at Children’s Hospital/Harvard Medical School, where in 1991 she became an Assistant Professor of Pediatrics. In 1999, she moved to the University of Arizona where she currently is a Professor of Cellular and Molecular Medicine, the Associate Director of the Asthma and Airway Disease Research Center, and the Director of the Arizona Center for the Biology of Complex Diseases (ABCD). She is an elected member of the Association of American Physicians (AAP) and from 2005 to 2012 was the Associate Editor for Genetics of The Journal of Allergy and Clinical Immunology. Dr. Vercelli’s research relies on both human and animal models and focuses on the environmental, genetic and epigenetic mechanisms that regulate allergic inflammation and asthma.
- Allergy & Immunology Specialist
- University of Florence
- Hematology Specialist
- University of Florence
- University of Florence
- Philip Fireman Lectureship
- 11th International Nemacolin Asthma Conference, Nemacolin, PA, USA, Fall 2016
- Guest Editor
- Current Opinions in Immunology, Fall 2015
- Giles Filley Lectureship
- Aspen Lung Conference/University of Colorado, Summer 2015
No activities entered.
DissertationCMM 920 (Fall 2016)
Lab Research RotationGENE 795A (Fall 2016)
Prin of Cell BiologyCMM 577 (Fall 2016)
Prin of Cell BiologyMCB 577 (Fall 2016)
DissertationCMM 920 (Spring 2016)
Pblms Bio Cmplx DiseasesCMM 595H (Spring 2016)
Pblms Bio Cmplx DiseasesGENE 595H (Spring 2016)
Pblms Bio Cmplx DiseasesIMB 595H (Spring 2016)
Pblms Bio Cmplx DiseasesMCB 595H (Spring 2016)
Pblms Bio Cmplx DiseasesPCOL 595H (Spring 2016)
DissertationCMM 920 (Fall 2015)
Lab Research RotationGENE 795A (Fall 2015)
Prin of Cell BiologyCMM 577 (Fall 2015)
Prin of Cell BiologyMCB 577 (Fall 2015)
DissertationCMM 920 (Spring 2015)
Pblms Bio Cmplx DiseasesCMM 595H (Spring 2015)
Pblms Bio Cmplx DiseasesIMB 595H (Spring 2015)
Pblms Bio Cmplx DiseasesMCB 595H (Spring 2015)
Pblms Bio Cmplx DiseasesPCOL 595H (Spring 2015)
ResearchCMM 900 (Spring 2015)
DissertationCMM 920 (Fall 2014)
Prin of Cell BiologyCMM 577 (Fall 2014)
Prin of Cell BiologyMCB 577 (Fall 2014)
ResearchCMM 900 (Fall 2014)
DissertationCMM 920 (Spring 2014)
Introduction to ResearchMCB 795A (Spring 2014)
Pblms Bio Cmplx DiseasesCMM 595H (Spring 2014)
Pblms Bio Cmplx DiseasesMCB 595H (Spring 2014)
Pblms Bio Cmplx DiseasesPCOL 595H (Spring 2014)
Directed RsrchMCB 492 (Fall 2013)
Introduction to ResearchMCB 795A (Fall 2013)
Prin of Cell BiologyCMM 577 (Fall 2013)
Prin of Cell BiologyMCB 577 (Fall 2013)
ResearchCMM 900 (Fall 2013)
- Vercelli, D., & DeVries, A. (2016). DNA methylation biomarkers in asthma and allergy. In Epigenetic Biomarkers and Diagnostics(pp 331-350). Academic Press.
- 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.More infoMexican-born children living in the United States have a lower prevalence of asthma than other US children. Although children of Mexican descent near the Arizona (AZ)-Sonora border are genetically similar, differences in environmental exposures might result in differences in asthma prevalence across this region.
- 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. Editorial. Am. J. Respir. Crit. Care Med..
- Vercelli, D. (2016). Does epigenetics play a role in human asthma?. Allergol. Int., 65, 123-126.
- 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.More infoAsthma 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.More infoThe 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.
- Martinez, F. D., & Vercelli, D. (2013). Asthma. Lancet (London, England), 382(9901), 1360-72.More infoAsthma 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.
- 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.More infoMultiple 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.More infoSOCS-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.More infoMany 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.More infoThe 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. The Journal of biological chemistry, 285(11), 8256-67.More infoExpression 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.More infoAsthma 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.More infoThe 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.More infoThe 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... The Journal of allergy and clinical immunology, 125(2), 347-8.
- von Mutius, E., & Vercelli, D. (2010). Farm living: effects on childhood asthma and allergy. Nature reviews. Immunology, 10(12), 861-8.More infoNumerous 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.More infoIL-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.More infoA 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. (2008). Advances in asthma and allergy genetics in 2007. The Journal of allergy and clinical immunology, 122(2), 267-71.More infoThis 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.More infoAsthma 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.
- 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.
- 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. (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.
- 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.
- Vercelli, D. (2009). Gene-environment interactions: the road less traveled by in asthma genetics. The Journal of allergy and clinical immunology.