Jesus Rivera-Nieves, M.D. is currently Professor of Medicine, member of the Inflammatory Bowel Disease Center at the University of California San Diego Medical Center and at the Veteran's Administration Hospital San Diego. Dr. Rivera-Nieves research focuses on new treatment strategies for inflammatory bowel disease (IBD) using unique mouse models that develop Crohn's-like terminal ileitis. Prior to joining the UCSD GI program, Dr. Rivera-Nieves was part of the Mucosal Inflammation Program at the University of Colorado Denver. He began his medical training in San Juan at the University of Puerto Rico Medical Sciences Campus and later joined the Howard Hughes-NIH research scholars program. After completing his MD, Dr. Rivera-Nieves completed his residency at the University of Maryland and then trained as a Gastroenterology and Hepatology research fellow at the University of Virginia. Dr. Rivera-Nieves basic research program on leukocyte traffic has been supported by NIDDK, CCFA and a VA Merit Research award. He has published over 60 manuscripts in peer-reviewed journals. He also chaired the Diversity Committee of the American Gastroenterology Association and has an Adjunct appointment at the Division of Inflammation Biology of the La Jolla Institute of Allergy and Immunology.
The inflammatory bowel diseases (IBD) affect over a million people in North America and their incidence is on the rise. These 2 chronic inflammatory conditions affect distinct intestinal segments and while ulcerative colitis involves strictly the large intestine, Crohn's disease may appear anywhere in the alimentary tract, from the mouth to the anus. Lymphocytes (T cells) are imprinted by dendritic cells with a cytokine (e.g. Th1, Th17) and homing program (e.g. CCR9, α4β7 integrin) and are in great part responsible for the perpetuation of IBD. The imprinting mechanisms that result in the expression of specific surface molecules required for the regional localization of IBD are only partially understood.
The goal of our research if to further understand how are immune cells to home specifically to distinct intestinal segments to explain the regional localization of the 2 main IBDs.
We utilize a variety of mouse models of IBD from simple chemically-induced injury models (e.g. DSS) to immunologically-manipulated models (i.e. CD45Rbhightransfer) to spontaneous chronic models of colitis and Crohn's-like ileitis (i.e. TNFΔARE, SAMP1/Yit) and patient-derived samples.
Our long-term goals
Blocking traffic has been proven efficacious for the treatment of Crohn's disease, through the use of antibodies against integrins (i.e. natalizumab). However, in certain patients serious complications from this therapy have occurred. Further understanding the mechanisms of traffic to the intestine will allow us to fine-tune this strategy for both efficacy and safety.