title: Regulatory T cells and intestinal homeostasis.
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.
authors.affiliation: Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, UK.
authors.forename: Janine L
authors.initials: JL
authors.lastname: Coombes
authors.forename: Nicholas J
authors.initials: NJ
authors.lastname: Robinson
authors.forename: Kevin J
authors.initials: KJ
authors.lastname: Maloy
authors.forename: Holm H
authors.initials: HH
authors.lastname: Uhlig
authors.forename: Fiona
authors.initials: F
authors.lastname: Powrie
mesh_terms: D000818:Animals; D016207:Cytokines / Q000276:immunology; D006706:Homeostasis; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000209:etiology / Q000276:immunology* / Q000473:pathology*; D008221:Lymphoid Tissue / Q000166:cytology / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology / Q000276:immunology*
chemical_list: D016207:Cytokines