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.