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炎症性肠病过程中结肠上皮细胞的死亡:CD95/Fas 及其以外的途径。

Cell death in the colonic epithelium during inflammatory bowel diseases: CD95/Fas and beyond.

机构信息

Ben May Department for Cancer Research, University of Chicago, Chicago, Illinois 60637, USA.

出版信息

Inflamm Bowel Dis. 2010 Jun;16(6):1071-6. doi: 10.1002/ibd.21191.

DOI:10.1002/ibd.21191
PMID:20049945
Abstract

CD95 is a member of the death receptor family. It is a prototypical inducer of apoptosis that, upon binding of its cognate ligand (CD95L), forms a death-inducing signaling complex composed of adaptor molecules and initiator caspases that transmit the apoptosis signal. The CD95/CD95L system was implicated in the etiology of inflammatory bowel disease (IBD) based, primarily, on the finding that CD95 is highly expressed in the intestinal epithelial cells and that epithelial apoptosis is increased in IBD. In recent years it has been recognized that CD95, while playing an important role as an apoptosis-inducing receptor in the immune system, also has multiple nonapoptotic functions on nonimmune cells. This review critically discusses the data on the possible function of CD95 as an apoptosis-inducing receptor in IBD and discusses alternative mechanisms for epithelial cell loss in IBD.

摘要

CD95 是死亡受体家族的一员。它是一种典型的凋亡诱导物,在与其配体(CD95L)结合后,形成由衔接分子和起始半胱天冬酶组成的死亡诱导信号复合物,传递凋亡信号。CD95/CD95L 系统与炎症性肠病(IBD)的病因有关,主要基于以下发现:CD95 在肠上皮细胞中高度表达,IBD 中上皮细胞凋亡增加。近年来,人们认识到 CD95 作为免疫系统中诱导凋亡的受体具有重要作用,但在非免疫细胞上也具有多种非凋亡功能。本文批判性地讨论了 CD95 作为诱导凋亡受体在 IBD 中的可能作用的相关数据,并讨论了 IBD 中上皮细胞丢失的替代机制。

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