Toll-like Receptors in Inflammatory Bowel Diseases: A Decade Later

被引:281
作者
Cario, Elke [1 ,2 ]
机构
[1] Univ Duisburg Essen, Div Gastroenterol & Hepatol, Univ Hosp Essen, Inst Grp 1, D-45147 Essen, Germany
[2] Univ Duisburg Essen, Sch Med, D-45147 Essen, Germany
关键词
Toll-like receptor; inflammatory bowel disease; review; innate immunity; host defense; intestinal mucosa; Crohn's disease; ulcerative colitis; INTESTINAL EPITHELIAL-CELLS; PROINFLAMMATORY GENE-EXPRESSION; GENOME-WIDE ASSOCIATION; SEGMENTED FILAMENTOUS BACTERIA; ENDOPLASMIC-RETICULUM STRESS; INNATE IMMUNE-RESPONSES; CROHNS-DISEASE; DENDRITIC CELLS; ULCERATIVE-COLITIS; INTERLEUKIN-10-DEFICIENT MICE;
D O I
10.1002/ibd.21282
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:1583 / 1597
页数:15
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