Immunopathogenesis of inflammatory bowel disease.

Julien Matricon, Nicolas Barnich, Denis Ardid
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引用次数: 127

Abstract

Inflammatory bowel disease (IBD) is a group of idiopathic, chronic and relapsing inflammatory conditions of the gastrointestinal tract. Familial and epidemiological studies have stressed the involvement of genetic factors and have also shown the critical role of environmental factors such as sanitation and hygiene in the development of IBD. However, the molecular mechanisms of intestinal inflammation in IBD have long remained unknown. In recent years, the study of susceptibility genes involved in the detection of bacterial components and in the regulation of the host immune response has shed light onto the potential role of intestinal pathogens and gut flora in IBD immunobiology. This review presents current knowledge on intestinal epithelial barrier alterations and on dysfunction of mucosal innate and acquired immune responses in IBD. The data support the etiological hypothesis which argues that pathogenic intestinal bacteria and/or infectious agents initiate and perpetuate the inflammation of the gut through disruption of tolerance towards the commensal microbiota in an individual with genetic vulnerability.

Abstract Image

Abstract Image

炎症性肠病的免疫发病机制。
炎症性肠病(IBD)是一组特发性、慢性和复发性胃肠道炎症。家族和流行病学研究强调了遗传因素的参与,也显示了环境因素如环境卫生和个人卫生在IBD发展中的关键作用。然而,IBD肠道炎症的分子机制长期以来仍不清楚。近年来,对参与细菌成分检测和宿主免疫反应调控的易感基因的研究,揭示了肠道病原体和肠道菌群在IBD免疫生物学中的潜在作用。本文综述了目前关于肠上皮屏障改变以及肠炎性疾病中粘膜先天和获得性免疫反应功能障碍的研究进展。这些数据支持病原学假说,即在具有遗传易感性的个体中,致病性肠道细菌和/或感染性病原体通过破坏对共生微生物群的耐受性而引发并延续肠道炎症。
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