Jeremy A. Goettel, Ph.D.
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Mechanisms regulating intestinal immunity
Dr. Jeremy Goettel earned his Ph.D. at Vanderbilt University in the Department of Cell and Developmental Biology under the direction of pediatric gastroenterologist Dr. D. Brent Polk where he worked on intestinal epithelial cell signaling downstream of the TNF receptor. He then pursued training in mucosal immunology in the laboratory of adult gastroenterologist Dr. Scott Snapper at Harvard Medical School and Boston Children’s Hospital. There he focused on mechanisms of intestinal immune homeostasis and cross-regulation of the host immune system with the intestinal microbiome. In pursuit of a translational platform in which to validate in vivo murine models, Dr. Goettel developed several humanized mouse strains to study human immunobiology and assess novel therapeutics for treating inflammatory bowel disease. Dr. Goettel was awarded the CCFA Shanti Sitaraman Young IBD Investigator Award in 2016 and the Young Investigator Award from the International Congress of Mucosal Immunology in 2017 and was recruited back to Vanderbilt University Medical Center to start his own laboratory. Dr. Goettel has been funded in part by industry partners Janssen and Merck and is currently funded through the Crohn’s and Colitis Foundation and the NIH, National Institute of Diabetes and Digestive and Kidney Diseases.
Research Information
Our lab is interested in understanding the mechanisms regulating intestinal immunity and what leads to dysregulation and disease as well as how gut microbes shape the mucosal immune system. In particular the cytokine interleukin-23 (IL23) is required for the development of many experimental models of inflammatory bowel disease (IBD) in mice and mutations in IL23 receptor (IL23R) have been identified as susceptibility or resistance factors for Crohn’s disease. We have developed several murine strains that will facilitate investigations into the role of IL23R signaling in a cell-specific manner using experimental models of IBD and inflammation-associated carcinogenesis. In addition, we have developed several humanized murine systems to model intestinal inflammation driven by human immune cells and new models enabling engraftment of human tumors with autologous immune cells to assess combination therapies and immune activation. We hope that these strategies will be informative for clinical management and pave the way towards precision medicine.
