Maloy, K. J. , Salaun, L., Cahill, R., Dougan, G., Saunders, N. J. and Powrie, F. (2003) CD4+CD25+ T(R) cells suppress innate immune pathology through cytokine-dependent mechanisms. Journal of Experimental Medicine, 197(1), pp. 111-119. (doi: 10.1084/jem.20021345) (PMID:12515818) (PMCID:PMC2193798)
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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.
Item Type: | Articles |
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Status: | Published |
Refereed: | Yes |
Glasgow Author(s) Enlighten ID: | Maloy, Professor Kevin |
Authors: | Maloy, K. J., Salaun, L., Cahill, R., Dougan, G., Saunders, N. J., and Powrie, F. |
College/School: | College of Medical Veterinary and Life Sciences > School of Infection & Immunity |
Journal Name: | Journal of Experimental Medicine |
Publisher: | Rockefeller University Press |
ISSN: | 0022-1007 |
ISSN (Online): | 1540-9538 |
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