1. Immunopathogenesis of Colitis-Associated Cancer in an Animal Model.
- Author
-
Zhao JL, Xiao CX, and Guleng B
- Subjects
- Animals, Colitis metabolism, Colitis pathology, Cytokines metabolism, Humans, Mice, Neoplasms metabolism, Colitis chemically induced, Disease Models, Animal, Immunity, Cellular immunology, Neoplasms etiology, Neoplasms pathology, T-Lymphocytes, Regulatory immunology
- Abstract
Chronic inflammation, such as that seen in patients with inflammatory bowel disease (IBD), greatly increases the risk of developing colon cancer. Growing evidence supports a role for T cell-mediated immune response and release of various cytokines in the pathogenesis of colitis-associated cancer (CAC). In fact, CD4+ effector T cells promote chronic inflammation associated with IBD through release of proinflammatory cytokines, which leads to initiation and progression of colon cancer. Furthermore, CD8+ T cells reduce tumor growth through cancer immunosurveillance, which can also contribute to intestinal inflammation and thereby might promote tumor growth. In contrast, regulatory T cells (Tregs) release the immunosuppressive cytokines IL-10, TGF-β and thus have protective effects in CAC. In addition, dendritic cells (DCs) are important components of antitumor immunity. Recently, a novel mouse model that was associated with repeated inflammation was established for investigating the immunopathogenesis of CAC. This review discusses the role of T cell-mediated immune response, and DCs and involved cytokines in the immunopathogenesis of CAC in an animal model, which may also provide future therapeutic targets in CAC.
- Published
- 2015
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