Immunopathogenesis of Colitis-Associated Cancer in an Animal Model

Crit Rev Eukaryot Gene Expr. 2015;25(3):245-51. doi: 10.1615/critreveukaryotgeneexpr.2015013885.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Colitis / chemically induced*
  • Colitis / metabolism
  • Colitis / pathology
  • Cytokines / metabolism
  • Disease Models, Animal*
  • Humans
  • Immunity, Cellular / immunology*
  • Mice
  • Neoplasms / etiology*
  • Neoplasms / metabolism
  • Neoplasms / pathology*
  • T-Lymphocytes, Regulatory / immunology*

Substances

  • Cytokines