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- W4313354012 abstract "Abstract Like many models of tissue-localized autoimmune disease, experimental autoimmune myocarditis (EAM) is mediated by Th17-directed pathology. The composition of cardiac infiltrates in EAM is predominantly monocytic, indicating that these cells are likely to be major inflammatory effectors in this disease process. In common with other Th17 autoimmune diseases, IFNγ-deficient mice develop very severe disease. We observed enhanced GM-CSF production from autoantigen-specific IFNγ-/- CD4+ cells, derived from the heart or spleen, suggesting that the induction of GM-CSF by Th17 cells controls the involvement of monocytes and macrophages in disease. After generating IFNγ-/-IL17A-/- double-knockout mice, we determined that the production of GM-CSF in CD4+ is driven by IL17 signaling. Towards this end, we generated bone marrow-derived macrophages (BMMϕ) in vitro, in the presence of GM-CSF, rather than M-CSF. Following adoptive transfer, recipients of GM-CSF BMMϕ developed more severe disease than controls. This severe disease was accompanied by enhanced fibrosis and compromised cardiac function. This novel report links GM-CSF control of macrophage differentiation to the functional consequences of Th17-mediated autoimmunity." @default.
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- W4313354012 date "2013-05-01" @default.
- W4313354012 modified "2023-09-26" @default.
- W4313354012 title "GM-CSF control of macrophage differentiation is a critical effector of Th17 responses in vivo (P4180)" @default.
- W4313354012 doi "https://doi.org/10.4049/jimmunol.190.supp.172.17" @default.
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