Guest guest Posted November 6, 2008 Report Share Posted November 6, 2008 Annu Rev Med. 2008 Oct 31. [Epub ahead of print] IL-23 and Autoimmunity: New Insights into the Pathogenesis of Inflammatory Bowel Disease. Abraham C, Cho JH Section of Digestive Diseases, Departments of Medicine, Yale University,New Haven, Connecticut 06520; email: clara.abraham@.... The intestinal immune system has the challenge of maintaining both a state of tolerance toward intestinal antigens and the ability to combat pathogens. This balance is partially achieved by reciprocal regulation of proinflammatory, effector CD4(+) T cells, and tolerizing, suppressive Treg subsets. Inflammatory bowel disease (IBD) comprises Crohn's disease (CD) and ulcerative colitis (UC). Genome-wide association studies have linked CD to a number of IL-23 pathway genes, notably IL23R (interleukin 23 receptor). Similar associations in IL-23 pathway genes have been observed in UC. IL23R is a key differentiation feature of CD4(+) Th17 cells, effector cells that are critical in mediating antimicrobial defenses. However, IL-23 and Th17 cell dysregulation can lead to end-organ inflammation. The differentiation of inflammatory Th17 cells and suppressive CD4(+) Treg subsets is reciprocally regulated by relative concentrations of TGFbeta, with the concomitant presence of proinflammatory cytokines favoring Th17 differentiation. The identification of IL-23 pathway and Th17 expressed genes in IBD pathogenesis highlights the importance of the proper regulation of the IL-23/Th17 pathway in maintaining intestinal immune homeostasis. PMID: 18976050. Quote Link to comment Share on other sites More sharing options...
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