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World J Gastroenterol. Jan 7, 2014; 20(1): 6-21
Published online Jan 7, 2014. doi: 10.3748/wjg.v20.i1.6
Immunopathology of inflammatory bowel disease
Kori L Wallace, Li-Bo Zheng, Yoshitake Kanazawa, David Q Shih
Kori L Wallace, Yoshitake Kanazawa, David Q Shih, F Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles CA 90048, United States
Li-Bo Zheng, Department of Gastroenterology, The Second Hospital of Hebei Medical University, Shijiazhuang 050000, Hebei Province, China
Author contributions: Wallace KL drafted and revised the article; Zheng LB and Kanazawa Y revised the article for intellectual content; Shih DQ revised the article for intellectual content and gave final approval of version to be published.
Supported by NIH KO8 DK093578; CCFA Career Development Award 3467 (DQS); F Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute
Correspondence to: David Q Shih, MD, PhD, F Widjaja Foundation, Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, 8700 Beverly Blvd, Suite 4066, Los Angeles CA 90048, United States. david.shih@csmc.edu
Telephone: +1-310-4237722 Fax: +1-310-4230224
Received: September 9, 2013
Revised: November 7, 2013
Accepted: November 28, 2013
Published online: January 7, 2014
Processing time: 123 Days and 22.4 Hours
Core Tip

Core tip: Inflammatory bowel disease (IBD) results from the complex interactions between susceptibility genes, the environment, the immune system, and the host’s microbiome. It is thought that either a mucosal susceptibility or a defect in sampling of gut luminal antigen leads to activation of the innate immune system that then recruits cells of the adaptive immune system leading to inflammation. This review will detail the interaction of these components in the immunopathogenesis of IBD.