Regulatory T cells and intestinal homeostasis
Article first published online: 16 MAR 2005
Volume 204, Issue 1, pages 184–194, April 2005
How to Cite
Coombes, J. L., Robinson, N. J., Maloy, K. J., Uhlig, H. H. and Powrie, F. (2005), Regulatory T cells and intestinal homeostasis. Immunological Reviews, 204: 184–194. doi: 10.1111/j.0105-2896.2005.00250.x
- Issue published online: 16 MAR 2005
- Article first published online: 16 MAR 2005
Summary: 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-β, 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.