Induced and Natural Regulatory T Cells in the Development of Inflammatory Bowel Disease

Section of Rheumatology, Department of Pediatrics, Medical College of Wisconsin, Milwaukee, Wisconsin.
Inflammatory Bowel Diseases (Impact Factor: 4.46). 05/2013; 19(8). DOI: 10.1097/MIB.0b013e318281f5a3
Source: PubMed


: The mucosal immune system mediates contact between the host and the trillions of microbes that symbiotically colonize the gastrointestinal tract. Failure to tolerate the antigens within this "extended self" can result in inflammatory bowel disease (IBD). Within the adaptive immune system, the most significant cells modulating this interaction are Foxp3 regulatory T (Treg) cells. Treg cells can be divided into 2 primary subsets: "natural" Treg cells and "adaptive" or "induced" Treg. Recent research suggests that these subsets serve to play both independent and synergistic roles in mucosal tolerance. Studies from both mouse models and human patients suggest that defects in Treg cells can play distinct causative roles in IBD. Numerous genetic, microbial, nutritional, and environmental factors that associate with IBD may also affect Treg cells. In this review, we summarize the development and function of Treg cells and how their regulatory mechanisms may fail, leading to a loss of mucosal tolerance. We discuss both animal models and studies of patients with IBD suggesting Treg cell involvement in IBD and consider how Treg cells may be used in future therapies.

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Available from: Christopher G Mayne, Jun 27, 2014
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    • "Impaired mucosal regulatory T cell function has been implicated in the pathogenesis of inflammatory bowel disease [28] but the effect of C. difficile infection on T cell function in patients with ulcerative colitis and Crohn’s disease remains to be determined. It is possible that C. difficile toxin-induced cytokine expression in macrophages [29] may lead to resistance of effector T cells to suppression by regulatory T cells and thereby lead to exacerbation of mucosal inflammation in inflammatory bowel disease. "
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