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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.

Original publication

DOI

10.1084/jem.20021345

Type

Journal article

Journal

The Journal of experimental medicine

Publication Date

01/2003

Volume

197

Pages

111 - 119

Addresses

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford, OX1 3RE, United Kingdom. kevin.maloy@path.ox.ac.uk

Keywords

Intestines, T-Lymphocytes, Animals, Mice, Helicobacter Infections, Inflammation, Transforming Growth Factor beta, Receptors, Interleukin-2, Antigens, CD4, Interleukin-10, Cytokines, Adoptive Transfer, Immunity, Innate