Dr. Dominic Ciavatta has been promoted to Research Professor in the Department of Genetics, effective November 1, 2023.
Dr. Ciavatta received his B.S. in Biology from Oglethorpe University in 1991 followed by a Ph.D. in Biochemistry from University of Alabama at Birmingham in 1999. He then completed postdoctoral training in the Department of Pathology and Laboratory Medicine at UNC-Chapel Hill (2000-2005). Dr. Ciavatta was appointed Research Associate in the UNC Department of Genetics in 2005, promoted to Research Assistant Professor in 2007 and to Research Associate Professor in 2014.
Enabled by his faculty position in Genetics and a research collaboration with Dr. Ronald Falk in the UNC Kidney Center, Dr. Ciavatta has built strong collaborations that support his research focused on the genetics and epigenetics of autoimmunity. Dr. Ciavatta’s research program is multi-tiered and has made important contributions to our understanding of antineutrophilic cytoplasmic antibody (ANCA) associated vasculitis. He has Identified an association between a genetic variant and expression of the PRTN3 gene, which encodes the autoantigen PR3, and increased risk of relapse in patients with PR3-ANCA vasculitis who carry the genetic variant. Through his investigations, he proposed a pathogenic role for autoantigen gene expression by demonstrating autoantigen gene expression correlated with ANCA mediated neutrophil activation. He identified a link between autoantigen gene expression and ANCA mediated neutrophil activation that supports the model that ANCA pathogenesis involves regulation of the autoantigen, not just the presence of autoantibody. His lab discovered that a change in DNA methylation at a specific gene in patients with ANCA vasculitis was associated with a probability of patients to relapse and identified an alternative gene isoform for the ANCA autoantigen, PR3, that is expressed in patients with ANCA disease. They went on to identify differences in chromatin modifications between healthy individuals and patients with ANCA disease, which implicates epigenetic control of expression of autoantigen genes. The translational impact of his research is important for designing new treatments for ANCA vasculitis sufferers.