Regulatory T cells and intestinal homeostasis

Immunol Rev. 2005 Apr;204:184-94. doi: 10.1111/j.0105-2896.2005.00250.x.

Abstract

Murine models of inflammatory bowel disease (IBD) are useful tools for the study of the pathogenesis and regulation of intestinal inflammation. Colitis can be induced in immune-deficient mice following transfer of populations of T cells or following infection with Helicobacter hepaticus and other intestinal pathogens. In these situations, colitis occurs as a result of the absence of a specialized population of regulatory cells, as transfer of CD4(+)CD25(+) T cells prevents disease. Importantly, from a clinical perspective, CD4(+)CD25(+) T cells can also reverse an established colitis. CD4(+)CD25(+) T cells proliferate both in the secondary lymphoid organs and at the site of inflammation, suggesting that regulation occurs both locally and systemically. CD4(+)CD25(+) T cells are not only capable of regulating other T cells but are also capable of suppressing components of the innate immune system. Control of colitis is dependent on the presence of the immunosuppressive cytokines interleukin-10 and transforming growth factor-beta, although their roles are divergent and complex. Regulatory T cells represent one of the host's mechanisms to prevent immune pathology during chronic immune stimulation. Enhancement of regulatory T-cell activity may be useful to control autoreactive T-cell responses and inhibit harmful inflammatory diseases such as asthma and IBD.

Publication types

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

MeSH terms

  • Animals
  • Cytokines / immunology
  • Homeostasis*
  • Humans
  • Inflammatory Bowel Diseases / etiology
  • Inflammatory Bowel Diseases / immunology*
  • Inflammatory Bowel Diseases / pathology*
  • Lymphoid Tissue / cytology
  • Lymphoid Tissue / immunology
  • T-Lymphocytes / cytology
  • T-Lymphocytes / immunology*

Substances

  • Cytokines