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Intestinal epithelial TOLLerance versus inTOLLerance of commensals.肠道上皮对共生菌的耐受与不耐受
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Nod2 mutation in Crohn's disease potentiates NF-kappaB activity and IL-1beta processing.克罗恩病中的Nod2突变增强了核因子κB活性和白细胞介素-1β的加工过程。
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Nod2-dependent regulation of innate and adaptive immunity in the intestinal tract.Nod2对肠道固有免疫和适应性免疫的调控
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Gut. 2005 Feb;54(2):308; author reply 309.

细菌与肠黏膜细胞的相互作用：Toll样受体和NOD2

Bacterial interactions with cells of the intestinal mucosa: Toll-like receptors and NOD2.

作者信息

Cario E

机构信息

University Hospital of Essen, Division of Gastroenterology and Hepatology, Institutsgruppe I, Virchowstr 171; D-45147 Essen, Germany.

出版信息

Gut. 2005 Aug;54(8):1182-93. doi: 10.1136/gut.2004.062794. Epub 2005 Apr 19.

DOI:10.1136/gut.2004.062794
PMID:15840688
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1774880/
Abstract

Toll-like receptors (TLR) and NOD2 are emerging as key mediators of innate host defence in the intestinal mucosa, crucially involved in maintaining mucosal as well as commensal homeostasis. Recent observations suggest new (patho-) physiological mechanisms of how functional versus dysfunctional TLRx/NOD2 pathways may oppose or favour inflammatory bowel disease (IBD). In health, TLRx signalling protects the intestinal epithelial barrier and confers commensal tolerance whereas NOD2 signalling exerts antimicrobial activity and prevents pathogenic invasion. In disease, aberrant TLRx and/or NOD2 signalling may stimulate diverse inflammatory responses leading to acute and chronic intestinal inflammation with many different clinical phenotypes.

摘要

Toll样受体（TLR）和NOD2正逐渐成为肠道黏膜固有宿主防御的关键介质，对维持黏膜以及共生菌的稳态至关重要。最近的观察结果提示了功能性与功能失调性TLRx/NOD2通路可能如何对抗或促进炎症性肠病（IBD）的新的（病理）生理机制。在健康状态下，TLRx信号传导可保护肠道上皮屏障并赋予共生菌耐受性，而NOD2信号传导则发挥抗菌活性并防止病原体入侵。在疾病状态下，异常的TLRx和/或NOD2信号传导可能刺激多种炎症反应，导致具有许多不同临床表型的急性和慢性肠道炎症。