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Immunobiology of T Cells in Inflammatory Bowel Disease

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Crohn's Disease and Ulcerative Colitis

Abstract

T lymphocytes play a central role in the pathogenesis of human as well as animal models of inflammatory bowel diseases (IBDs). In murine models, inflammation can be induced by adoptive transfer of T cells into appropriate hosts. Effector T cells, which mediate inflammation, can be classified by unique cytokine expression signatures. Crohn’s disease has been associated with Th1 and Th17 cytokine secretion, whereas Th2 cytokines have been associated in ulcerative colitis. However, not all T cells are pathogenic; some normally function to suppress immune responses through diverse mechanisms including the secretion of anti-inflammatory cytokines. Naturally occurring regulatory T cells develop in the thymus, whereas those that are generated in the periphery or in vitro are called “inducible” regulatory T cells, which can be further categorized by the cytokines they secrete and the specific methods by which they have been generated. In murine models, a qualitative or quantitative defect in regulatory T cells can lead to colitis development, but there does not appear to be an obvious defect in regulatory T-cell number or function in IBDs. Effector and regulatory T-cell localization (homing) to mucosal tissues is facilitated by the expression of unique combinations of specific cell surface molecules. Therapies preventing T-cell homing to the gut have been found effective for both Crohn’s disease as well as ulcerative colitis. Understanding how T cells can mediate or prevent intestinal inflammation may lead to more effective treatments, such as those that may enhance regulatory T-cell number and/or function.

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Correspondence to Scott B. Snapper MD, PhD .

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Snapper, S.B., Nguyen, D.D. (2012). Immunobiology of T Cells in Inflammatory Bowel Disease. In: Baumgart, D. (eds) Crohn's Disease and Ulcerative Colitis. Springer, Boston, MA. https://doi.org/10.1007/978-1-4614-0998-4_11

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  • DOI: https://doi.org/10.1007/978-1-4614-0998-4_11

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