Dr. Iryna Pinchuk is currently an Associate Professor in the Division of Gastroenterology and Hepatology in the Department of Internal Medicine at The University of Texas Medical Branch (UTMB) in Galveston. She earned her PhD degree in Food and Biological Sciences from the University of Bordeaux I located in Talence, France. She then did postdoctoral fellowship at UT Health Center at Tyler, Texas and at UTMB at Galveston, Texas. Dr. Pinchuk's research during her postdoctoral fellowship at UTMB was supported by Crohn's & Colitis Foundation of America. She was promoted to Assistant Professor 2009. Her current research is supported by the American Gastroenterological Association (AGA Research Scholarship Award 2009-2011). Dr Pinchuk is co-author of a patent and has co-authored over 25 peer-reviewed journal articles and reviews.
Dr. Pinchuk's research interests are in the regulation of the human mucosal immune responses in acute and chronic inflammation, in particularly those involved in the progression of the inflammatory bowel disease (IBD) and colorectal cancer (CRC). A key event in an immune response is antigen recognition. Dr. Pinchuk has been characterizing a population of earlier non appreciated non professional antigen presenting cells (APCs), known as intestinal myofibroblasts/fibroblasts (IMFs or stromal cells) that are abundant in the human intestine and serve as a suppressor of acute inflammatory responses during mucosal tolerance. Currently, her studies are focused on the understanding of: (1) how different CD4+ T cell subtypes (in particularly, Th1, 2,17, 22 and CD4+ CD25high FoxP3+ regulatory T cells) are regulated by the IMFs when compare to professional APCs and epithelial cells; (2) how those T cell populations affect the phenotype and function of the stromal cells in gastro-intestinal tract; (3) how the stromal cells immusuppressive function is disrupted during acute and chronic inflammatory processes. Her research goal is to understand how the dysregulation of the interaction between those cells contribute to the disruption of the GI mucosal immune balance leading to the chronic inflammation that may results in the initiation of cancerogenesis during IBD and, finally, to CRC progression.