Abreu Maria T, Sparrow Miles P
Inflammatory Bowel Disease Center, Mount Sinai School of Medicine, 1 East 100th Street, Box 1069, New York, NY 10029, USA.
Mt Sinai J Med. 2006 Dec;73(8):1067-73.
The idiopathic inflammatory bowel diseases (IBDs), broadly classified as either Crohn's disease (CD) or ulcerative colitis (UC), are caused by a dysregulated mucosal immune response to a luminal antigen, possibly a bacterium, in a genetically predisposed host. A rapid expansion of knowledge in recent years has greatly increased our understanding of the pathophysiology of these disorders. For example, the relatively recent discovery of the NOD2 gene, a protein involved in bacterial sensing, has provided further evidence of the complex interplay between hosts and microbes in Crohn's disease. Significant recent advances have also occurred with the discovery of the role of Toll-like receptors and dendritic cells in the development of gut inflammation, and the role of proinflammatory cytokines in the development and potentiation of gut inflammation. This article presents an update on these key developments and emphasizes the translational aspects of research that are directly related to patient care.
特发性炎症性肠病（IBDs）大致分为克罗恩病（CD）或溃疡性结肠炎（UC），是由遗传易感性宿主对管腔抗原（可能是一种细菌）的黏膜免疫反应失调引起的。近年来知识的迅速扩展极大地增进了我们对这些疾病病理生理学的理解。例如，相对较新发现的NOD2基因（一种参与细菌感知的蛋白质），为克罗恩病中宿主与微生物之间复杂的相互作用提供了进一步证据。最近，随着Toll样受体和树突状细胞在肠道炎症发展中的作用以及促炎细胞因子在肠道炎症发展和增强中的作用的发现，也取得了重大进展。本文介绍了这些关键进展的最新情况，并强调了与患者护理直接相关的研究转化方面。
