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• W2137618875 endingPage "3669" @default.
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• W2137618875 abstract "A new class of inflammatory CD4(+) T cells that produce interleukin-17 (IL-17) (termed Th17) has been identified, which plays a critical role in numerous inflammatory conditions and autoimmune diseases. The active form of vitamin D, 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)], has a direct repressive effect on the expression of IL-17A in both human and mouse T cells. In vivo treatment of mice with ongoing experimental autoimmune encephalomyelitis (EAE; a mouse model of multiple sclerosis) diminishes paralysis and progression of the disease and reduces IL-17A-secreting CD4(+) T cells in the periphery and central nervous system (CNS). The mechanism of 1,25(OH)(2)D(3) repression of IL-17A expression was found to be transcriptional repression, mediated by the vitamin D receptor (VDR). Transcription assays, gel shifting, and chromatin immunoprecipitation (ChIP) assays indicate that the negative effect of 1,25(OH)(2)D(3) on IL-17A involves blocking of nuclear factor for activated T cells (NFAT), recruitment of histone deacetylase (HDAC), sequestration of Runt-related transcription factor 1 (Runx1) by 1,25(OH)(2)D(3)/VDR, and a direct effect of 1,25(OH)(2)D(3) on induction of Foxp3. Our results describe novel mechanisms and new concepts with regard to vitamin D and the immune system and suggest therapeutic targets for the control of autoimmune diseases." @default.
• W2137618875 created "2016-06-24" @default.
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• W2137618875 date "2011-09-01" @default.
• W2137618875 modified "2023-10-01" @default.
• W2137618875 title "1,25-Dihydroxyvitamin D₃ Ameliorates Th17 Autoimmunity via Transcriptional Modulation of Interleukin-17A" @default.
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• W2137618875 doi "https://doi.org/10.1128/mcb.05020-11" @default.
• W2137618875 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3165548" @default.
• W2137618875 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21746882" @default.
• W2137618875 hasPublicationYear "2011" @default.
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