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©2008 The WJG Press and Baishideng. All rights reserved.
World J Gastroenterol. Jan 21, 2008; 14(3): 390-400
Published online Jan 21, 2008. doi: 10.3748/wjg.14.390
Published online Jan 21, 2008. doi: 10.3748/wjg.14.390
Immunopathogenesis of inflammatory bowel disease
David Q Shih, Stephan R Targan, Cedars-Sinai Inflammatory Bowel Disease Center, Los Angeles, CA, United States
David Q Shih, Department of Medicine, Division of Digestive Diseases, University of California, Los Angeles, CA, United States
Correspondence to: Stephan R Targan, MD, Cedars-Sinai Inflammatory Bowel Disease Center, 8700 Beverly Blvd., Suite D4063, Los Angeles, CA 90048, United States. targans@cshs.org
Telephone: +1-310-4237724
Fax: +1-310-4230224
Received: May 16, 2007
Revised: July 4, 2007
Published online: January 21, 2008
Revised: July 4, 2007
Published online: January 21, 2008
Abstract
Crohn’s disease and ulcerative colitis are chronic relapsing immune mediated disorders that results from an aberrant response to gut luminal antigen in genetically susceptible host. The adaptive immune response that is then triggered was widely considered to be a T-helper-1 mediated condition in Crohn’s disease and T-helper-2 mediated condition in ulcerative colitis. Recent studies in animal models, genome wide association, and basic science has provided important insights in in the immunopathogenesis of inflammatory bowel disease, one of which was the characterization of the interleukin-23/Th-17 axis.