TY - JOUR AU - Maloy, KJ AU - Salaun, L AU - Cahill, R AU - Dougan, G AU - Saunders, NJ AU - Powrie, F Y2 - 2021/02/04 Y1 - 2003/01/06 SN - 0022-1007 UR - http://hdl.handle.net/11343/259503 AB - CD4(+)CD25(+) regulatory T (T(R)) cells can inhibit a variety of autoimmune and inflammatory diseases, but the precise mechanisms by which they suppress immune responses in vivo remain unresolved. Here, we have used Helicobacter hepaticus infection of T cell-reconstituted recombination-activating gene (RAG)(-/-) mice as a model to study the ability of CD4(+)CD25(+) T(R) cells to inhibit bacterially triggered intestinal inflammation. H. hepaticus infection elicited both T cell-mediated and T cell-independent intestinal inflammation, both of which were inhibited by adoptively transferred CD4(+)CD25(+) T(R) cells. T cell-independent pathology was accompanied by activation of the innate immune system that was also inhibited by CD4(+)CD25(+) T(R) cells. Suppression of innate immune pathology was dependent on T cell-derived interleukin 10 and also on the production of transforming growth factor beta. Thus, CD4(+)CD25(+) T(R) cells do not only suppress adaptive T cell responses, but are also able to control pathology mediated by innate immune mechanisms. LA - eng PB - Rockefeller University Press T1 - CD4+CD25+ T(R) cells suppress innate immune pathology through cytokine-dependent mechanisms. DO - 10.1084/jem.20021345 IS - Journal of Experimental Medicine VL - 197 IS - 1 SP - 111-119 L1 - /bitstream/handle/11343/259503/PMC2193798.pdf?sequence=1&isAllowed=y ER -