Immunopathology of inflammatory bowel disease

作     者：Kori L Wallace Li-Bo Zheng Yoshitake Kanazawa David Q Shih 

作者机构：F Widjaja FoundationInflammatory Bowel and Immunobiology Research InstituteCedars-Sinai Medical CenterLos Angeles CA 90048United States Department of GastroenterologyThe Second Hospital of Hebei Medical University 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2014年第20卷第1期

页      面：6-21页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

基　　金：Supported by NIH KO8 DK093578 CCFA Career Development Award 3467(DQS) F Widjaja Foundation Inflammatory Bowel and Immunobiology Research Institute 

主　　题：Inflammatory bowel disease, Crohn’ s disease, Ulcerative colitis, Microbiome, Autophagy, T helper 17, Innate immune system, Adaptive immune system, Innate lymphoid cells, TL1A 

摘      要：Inflammatory bowel disease (IBD) results from a complex series of interactions between susceptibility genes, the environment, and the immune system. The host microbiome, as well as viruses and fungi, play important roles in the development of IBD either by causing inflammation directly or indirectly through an altered immune system. New technologies have allowed researchers to be able to quantify the various components of the microbiome, which will allow for future developments in the etiology of IBD. Various components of the mucosal immune system are implicated in the pathogenesis of IBD and include intestinal epithelial cells, innate lymphoid cells, cells of the innate (macrophages/monocytes, neutrophils, and dendritic cells) and adaptive (T-cells and B-cells) immune system, and their secreted mediators (cytokines and chemokines). Either a mucosal susceptibility or defect in sampling of gut luminal antigen, possibly through the process of autophagy, leads to activation of innate immune response that may be mediated by enhanced toll-like receptor activity. The antigen presenting cells then mediate the differentiation of naïve T-cells into effector T helper (Th) cells, including Th1, Th2, and Th17, which alter gut homeostasis and lead to IBD. In this review, the effects of these components in the immunopathogenesis of IBD will be discussed.