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      Coordinated control of immunity to muscle stage Trichinella spiralis by IL-10, regulatory T cells, and TGF-beta.

      The Journal of Immunology Author Choice

      Animals, Cell Polarity, Cell Survival, Interferon-gamma, biosynthesis, Interleukin-10, deficiency, genetics, metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Myositis, immunology, parasitology, T-Lymphocytes, Regulatory, Th1 Cells, cytology, Th2 Cells, Transforming Growth Factor beta, Trichinella spiralis, Trichinellosis, pathology

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          Abstract

          We previously demonstrated that IL-10 is critical in the control of acute inflammation during development of Trichinella spiralis in the muscle. In this study, we use gene-targeted knockout mice, adoptive transfer of specific T cell populations, and in vivo Ab treatments to determine the mechanisms by which inflammation is controlled and effector T cell responses are moderated during muscle infection. We report that CD4(+)CD25(-) effector T cells, rather than CD4(+)CD25(+) regulatory T cells, suppress inflammation by an IL-10-dependent mechanism that limits IFN-gamma production and local inducible NO synthase induction. Conversely, we show that depletion of regulatory T cells during infection results in exaggerated Th2 responses. Finally, we provide evidence that, in the absence of IL-10, TGF-beta participates in control of local inflammation in infected muscle and promotes parasite survival.

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          17202367

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