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Colitis in mice lacking the common cytokine receptor gamma chain is mediated by IL-6-producing CD4+ T cells

Yasuyuki Kai1, Ichiro Takahashi, Hiromichi Ishikawa

  • 1Department of Mucosal Immunology, Osaka University, Japan.

Gastroenterology
|April 13, 2005
PubMed
Abstract

Insights

Aberrant T cells producing interleukin-6 (IL-6) drive colitis in mice with a common cytokine receptor gamma chain mutation. Blocking IL-6 prevents colitis by inducing apoptosis in these pathogenic T cells.

Area of Science:

  • Immunology
  • Gastroenterology
  • Cell Biology

Background:

  • Mice with a common cytokine receptor gamma chain (CR gamma -/Y) mutation spontaneously develop colitis.
  • Identifying the specific pathogenic elements triggering this inflammatory disease is crucial.

Purpose of the Study:

  • To elucidate and characterize aberrant T cells and their enteropathogenic cytokines in CR gamma -/Y mice with colitis.
  • To investigate the role of interleukin-6 (IL-6) in the development of colitis.

Main Methods:

  • Histological analysis, cell population assessment, T-cell receptor V beta usage, and cytokine production of lamina propria lymphocytes.
  • Treatment with anti-IL-6 receptor monoclonal antibody.
  • Adoptive transfer of splenic CD4+ T cells into SCID mice.

Main Results:

  • CR gamma -/Y mice exhibited thickened colons and mononuclear cell infiltration, specifically in euthymic mice.
  • Colonic CD4+ T cells exclusively produced IL-6 and expressed antiapoptotic proteins, utilizing specific T-cell receptor subsets (V beta 14).
  • Anti-IL-6 receptor treatment prevented colitis by inducing apoptosis in IL-6-producing CD4+ T cells; adoptive transfer of these cells induced colitis in SCID mice.

Conclusions:

  • Thymus-derived CD4+ T cells producing IL-6 are the primary cause of colitis in CR gamma -/Y mice.
  • Targeting IL-6 offers a potential therapeutic strategy for this type of colitis.

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