Division of Gastroenterology & Hepatology, University Hospital of Essen, and Medical School, University of Duisburg-Essen, Essen, Germany.
Inflamm Bowel Dis. 2010 Sep;16(9):1583-97. doi: 10.1002/ibd.21282.
Differential alteration of Toll-like receptor (TLR) expression in inflammatory bowel disease (IBD) was first described 10 years ago. Since then, studies from many groups have led to the current concept that TLRs represent key mediators of innate host defense in the intestine, involved in maintaining mucosal as well as commensal homeostasis. Recent findings in diverse murine models of colitis have helped to reveal the mechanistic importance of TLR dysfunction in IBD pathogenesis. It has become evident that environment, genetics, and host immunity form a multidimensional and highly interactive regulatory triad that controls TLR function in the intestinal mucosa. Imbalanced relationships within this triad may promote aberrant TLR signaling, critically contributing to acute and chronic intestinal inflammatory processes in IBD colitis and associated cancer.
10 年前首次描述了 Toll 样受体 (TLR) 在炎症性肠病 (IBD) 中的表达差异。从那时起，许多研究小组的研究导致了目前的概念，即 TLR 是肠道固有宿主防御的关键介质，参与维持黏膜和共生体的稳态。在不同的结肠炎小鼠模型中的最新发现有助于揭示 TLR 功能障碍在 IBD 发病机制中的机制重要性。显然，环境、遗传学和宿主免疫形成了一个多维且高度相互作用的调节三联体，控制肠道黏膜中的 TLR 功能。该三联体内部的不平衡关系可能会促进异常的 TLR 信号传递，这对 IBD 结肠炎和相关癌症中的急性和慢性肠道炎症过程有重要影响。
