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• W2011021908 endingPage "e0124802" @default.
• W2011021908 startingPage "e0124802" @default.
• W2011021908 abstract "Interferon (IFN)-β is a front-line therapy for the treatment of the relapsing-remitting form of multiple sclerosis. However, its immunosuppressive mechanism of function remains incompletely understood. While it has been proposed that IFN-β suppresses the function of inflammatory myelin antigen-reactive T cells by promoting the release of immunomodulatory cytokines such as IL-27 from antigen-presenting cells (APCs), its direct effects on inflammatory CD4+ Th1 cells are less clear. Here, we establish that IFN-β inhibits mouse IFN-γ+ Th1 cell function in the absence of APCs. CD4+ T cells express the type I interferon receptor, and IFN-β can suppress Th1 cell proliferation under APC-free stimulation conditions. IFN-β-treated myelin antigen-specific Th1 cells are impaired in their ability to induce severe experimental autoimmune encephalomyelitis (EAE) upon transfer to lymphocyte-deficient Rag1-/- mice. Polarized Th1 cells downregulate IFN-γ and IL-2, and upregulate the negative regulatory receptor Tim-3, when treated with IFN-β in the absence of APCs. Further, IFN-β treatment of Th1 cells upregulates phosphorylation of Stat1, and downregulates phosphorylation of Stat4. Our data indicate that IFN-γ-producing Th1 cells are directly responsive to IFN-β and point to a novel mechanism of IFN-β-mediated T cell suppression that is independent of APC-derived signals." @default.
• W2011021908 created "2016-06-24" @default.
• W2011021908 creator A5014418559 @default.
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• W2011021908 creator A5067628880 @default.
• W2011021908 creator A5081687175 @default.
• W2011021908 creator A5084120415 @default.
• W2011021908 date "2015-04-17" @default.
• W2011021908 modified "2023-10-15" @default.
• W2011021908 title "Interferon-β Suppresses Murine Th1 Cell Function in the Absence of Antigen-Presenting Cells" @default.
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• W2011021908 doi "https://doi.org/10.1371/journal.pone.0124802" @default.
• W2011021908 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4401451" @default.
• W2011021908 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25885435" @default.
• W2011021908 hasPublicationYear "2015" @default.
• W2011021908 type Work @default.
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