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The role of T‐regulatory cells and Toll‐like receptors in the pathogenesis of human inflammatory bowel disease
Author(s) -
Himmel Megan E.,
Hardenberg Gijs,
Piccirillo Ciriaco A.,
Steiner Theodore S.,
Levings Megan K.
Publication year - 2008
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2008.02939.x
Subject(s) - inflammatory bowel disease , immunology , immune system , pathogenesis , disease , flagellin , ulcerative colitis , biology , toll like receptor , regulatory t cell , receptor , inflammation , t cell , medicine , innate immune system , il 2 receptor , pathology , genetics
Summary 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.