The intestinal epithelium and underlying lamina propria contain T cells that play important roles in maintaining colonic homeostasis. These T cells mediate substantial and specific regulation to ensure that pathogenic microorganisms are eliminated while commensal bacteria are tolerated. There is considerable evidence supporting the notion that the altered ratio between Foxp3(+)CD4(+) T regulatory cells and T effector cells in the colonic microenvironment might contribute to the initiation and progression of inflammation and eventually development of colon cancer. Recent findings on the heterogeneity and plasticity of T regulatory cells, such as the identification of IL-17(+)Foxp3(+)CD4(+) and the RORγt(+)Foxp3(+)CD4(+) subsets, in patients with colorectal inflammation and cancer have provided a new twist in our understanding of the pathogenesis of colonic diseases. Phenotypic and functional properties of IL-17-producing Foxp3(+)CD4(+) T cells as well as the significant implications of these cells in the initiation and progression of colorectal diseases are discussed in this review.
Keywords: Colon cancer; IL-17; Inflammatory bowel disease; RORγt; T regulatory cells; Th17.
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