Abstract:: 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. (Inflamm Bowel Dis 2010)
1Division of Gastroenterology & Hepatology, University Hospital of Essen, and Medical School, University of Duisburg‐Essen, Essen, Germany
*Div. of Gastroenterology & Hepatology, University Hospital of Essen, Institutsgruppe I, Virchowstr. 171, D‐45147 Essen, Germany
Received 4 February 2010; Accepted 15 February 2010
Published online 12 April 2010 in Wiley Online Library (wileyonlinelibrary.com).
Grant sponsor: Crohn's and Colitis Foundation of America; Grant Number: 1790; Grant sponsor: Deutsche Forschungsgemeinschaft; Grant Number: CA226/4‐2.