Donata Vercelli
Director, Arizona Center for the Biology of Complex Diseases (ABCD)
Professor, BIO5 Institute
Professor, Cellular and Molecular Medicine
Professor, Genetics - GIDP
Associate Director, Asthma / Airway Disease Research Center
Primary Department
(520) 626-6387
Research Interest
Donata Vercelli, MD, is a Professor of Cellular and Molecular Medicine, the Associate Director of the Arizona Respiratory Center and the Director of the Arizona Center for the Biology of Complex Diseases. Her research work is at the cutting edge of the immunology and genetics of complex lung diseases. Her laboratory spans both human and animal models. After characterizing cellular and molecular events critical for the regulation of human IgE synthesis, she became interested in the mechanisms through which natural genetic variants modify susceptibility to complex diseases, particularly allergy and asthma. To this purpose, she developed innovative, unique mouse models in which distinct human haplotypes of asthma- and allergy-associated genes are carried by BAC transgenic mice and can be directly compared for their regulatory properties in vivo. The unexpected, essential mechanisms underpinning the involvement of Th2 cytokines in allergy and asthma revealed by this mouse model have been fully validated in human populations. Dr. Vercelli's work on the epigenetic regulation of Th2 cytokine expression in human neonatal T cells revealed novel facets of early life regulatory events and her continued interest in epigenetics has led to the first demonstration that neonatal DNA methylation signatures in innate immunoregulatory pathways predict asthma during childhood. Most recently, Dr. Vercelli has devised a highly innovative approach that combines epidemiologic, biochemical and mouse model studies to dissect the mechanisms underlying the asthma-protective and asthma-promoting effects of two distinct US farming environments (Amish and Hutterite). Such studies are likely to critically advance our knowledge about fundamental mechanisms of asthma pathogenesis.