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- W2002809074 abstract "Accumulation of IL-17-producing Th17 cells is associated with the development of multiple autoimmune diseases; however, the contribution of microRNA (miRNA) pathways to the intrinsic control of Th17 development remains unclear. Here, we demonstrated that miR-21 expression is elevated in Th17 cells and that mice lacking miR-21 have a defect in Th17 differentiation and are resistant to experimental autoimmune encephalomyelitis (EAE). Furthermore, we determined that miR-21 promotes Th17 differentiation by targeting and depleting SMAD-7, a negative regulator of TGF-β signaling. Moreover, the decreases in Th17 differentiation in miR-21-deficient T cells were associated with defects in SMAD-2/3 activation and IL-2 suppression. Finally, we found that treatment of WT mice with an anti-miR-21 oligonucleotide reduced the clinical severity of EAE, which was associated with a decrease in Th17 cells. Thus, we have characterized a T cell-intrinsic miRNA pathway that enhances TGF-β signaling, limits the autocrine inhibitory effects of IL-2, and thereby promotes Th17 differentiation and autoimmunity." @default.
- W2002809074 created "2016-06-24" @default.
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- W2002809074 date "2015-02-02" @default.
- W2002809074 modified "2023-10-12" @default.
- W2002809074 title "MicroRNA-21 promotes Th17 differentiation and mediates experimental autoimmune encephalomyelitis" @default.
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- W2002809074 doi "https://doi.org/10.1172/jci74347" @default.
- W2002809074 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4362225" @default.
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- W2002809074 hasPublicationYear "2015" @default.
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