The role of T-regulatory cells and Toll-like receptors in the pathogenesis of human inflammatory bowel disease
Article first published online: 5 SEP 2008
© 2008 The Authors Journal compilation © 2008 Blackwell Publishing Ltd
Volume 125, Issue 2, pages 145–153, October 2008
How to Cite
Himmel, M. E., Hardenberg, G., Piccirillo, C. A., Steiner, T. S. and Levings, M. K. (2008), The role of T-regulatory cells and Toll-like receptors in the pathogenesis of human inflammatory bowel disease. Immunology, 125: 145–153. doi: 10.1111/j.1365-2567.2008.02939.x
- Issue published online: 5 SEP 2008
- Article first published online: 5 SEP 2008
- Received 22 July 2008; revised 22 July 2008; accepted 29 July 2008.
- inflammatory bowel disease;
- Toll-like receptor;
- T regulatory cell
Two related chronic inflammatory diseases, Crohn’s disease and ulcerative colitis, are together often referred to as inflammatory bowel disease (IBD). Current treatment options are not curative, and patients face lifelong therapy and debilitation. IBD is thought to be the product of a combination of genetic and environmental factors that result in the abnormal regulation of immune responses. Experimental models have demonstrated that normal CD4+ T-regulatory (Treg) cell responses and commensal bacteria are required for the maintenance of gut immune homeostasis. Recent evidence that CD4+ T cells express Toll-like receptors (TLRs) and respond directly to TLR ligands, suggests that signals from commensal bacteria may directly affect T-cell responses in the gut. In this review, we focus on evidence that defects in Treg cells may underlie IBD in humans. In addition, we discuss evidence that direct signaling via TLRs to T cells can affect IBD and that T-cell-dependent responses to bacterial proteins, such as flagellin, are central to the aetiology of this disease.