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  -