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    CD4+CD25+ T(R) cells suppress innate immune pathology through cytokine-dependent mechanisms.

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    Author
    Maloy, KJ; Salaun, L; Cahill, R; Dougan, G; Saunders, NJ; Powrie, F
    Date
    2003-01-06
    Source Title
    Journal of Experimental Medicine
    Publisher
    Rockefeller University Press
    University of Melbourne Author/s
    Dougan, Gordon
    Affiliation
    Microbiology and Immunology
    Metadata
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    Document Type
    Journal Article
    Citations
    Maloy, K. J., Salaun, L., Cahill, R., Dougan, G., Saunders, N. J. & Powrie, F. (2003). CD4+CD25+ T(R) cells suppress innate immune pathology through cytokine-dependent mechanisms.. J Exp Med, 197 (1), pp.111-119. https://doi.org/10.1084/jem.20021345.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/259503
    DOI
    10.1084/jem.20021345
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2193798
    Abstract
    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.

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