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- W29207879 abstract "Abstract We and others have demonstrated the ability of granulocyte-macrophage colony-stimulating factor (GM-CSF) to induce and maintain semi-mature, tolerogenic DCs in vivo, and have shown that treatment could suppress autoimmunity by inducing CD4+CD25+ regulatory T cells (Tregs). In the current study, we have confirmed the critical role of Tregs in the therapeutic effects of GM-CSF both in vitro and in vivo utilizing extensive adoptive transfer experiments. Specifically, we show that Tregs from GM-CSF treated EAMG mice transferred to animals with EAMG suppress clinical disease more potently than equal numbers of Tregs from untreated mice. In addition, GM-CSF-induced-Tregs (GM-CSF iTregs) from EAMG mice potently and specifically suppress T cell proliferation induced by AChR, but do not alter T cell proliferation in response to irrelevant antigens to any greater extent than Tregs obtained from naive mice (so called natural Tregs [nTregs]). These results are consistent with the hypothesized mechanism of action of GM-CSF involving the mobilization of “semimature” dendritic cell precursors which, upon antigen (AChR) capture, initiate a suppression of the anti-AChR immune response, predominantly through the activation of AChR-specific iTregs. These preclinical findings provide important knowledge that may allow for clinical application of GM-CSF or related molecules to the treatment of human MG in the future." @default.
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- W29207879 date "2011-04-01" @default.
- W29207879 modified "2023-10-14" @default.
- W29207879 title "Regulatory T cells induced by GM-CSF suppress disease severity and selectively inhibit acetylcholine receptor-stimulated T cell responses in experimental myasthenia gravis (115.1)" @default.
- W29207879 doi "https://doi.org/10.4049/jimmunol.186.supp.115.1" @default.
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