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Critical Reviews™ in Eukaryotic Gene Expression
Facteur d'impact: 1.841 Facteur d'impact sur 5 ans: 1.927 SJR: 0.649 SNIP: 0.516 CiteScore™: 1.96

ISSN Imprimer: 1045-4403
ISSN En ligne: 2162-6502

Critical Reviews™ in Eukaryotic Gene Expression

DOI: 10.1615/CritRevEukaryotGeneExpr.2015013885
pages 245-251

Immunopathogenesis of Colitis-Associated Cancer in an Animal Model

Jun-Lin Zhao
Department of Anesthesiology, First Affiliated Hospital to Xiamen University, Xiamen, Fujian Province, China
Chuan-Xing Xiao
Department of Gastroenterology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian Province, China
Bayasi Guleng
Department of Gastroenterology, Zhongshan Hospital, Xiamen University, Xiamen, Fujian Province, China; Medical College of Xiamen University, Xiamen, Fujian Province, China, 361005

RÉSUMÉ

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.


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