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10.1016/j.bbi.2014.12.007

http://scihub22266oqcxt.onion/10.1016/j.bbi.2014.12.007
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C4414699!4414699!25499467
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pmid25499467      Brain+Behav+Immun 2015 ; 46 (ä): 44-9
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  • Analysis of TGF-?1 and TGF-?3 as Regulators of Encephalitogenic Th17 Cells: Implications for Multiple Sclerosis #MMPMID25499467
  • Lee PW; Yang Y; Racke MK; Lovett-Racke AE
  • Brain Behav Immun 2015[May]; 46 (ä): 44-9 PMID25499467show ga
  • The phenotype of the CD4+ T cells that mediate the CNS pathology in multiple sclerosis is still unclear, and yet a vital question for developing therapies. One of the conundrums is the role of TGF-? in the development of encephalitogenic Th17 cells. In the present study, TGF-?1 and TGF-?3 were directly compared in their capacity to promote the differentiation of myelin-specific Th17 cells that could induce experimental autoimmune encephalomyelitis (EAE). Myelin-specific CD4+ T cell receptor transgenic cells differentiated with antigen in the presence of IL-6+TGF-?1 or IL-6+TGF-?3 generated T cells that produced robust amounts of IL-17, but were incapable of inducing EAE when transferred into mice. Further analysis of these non-encephalitogenic Th17 cells found that they expressed lower amounts of GM-CSF or IL-23R, both molecules necessary for encephalitogenicity. Thus, TGF-?, irrespective of isoform, negatively regulates the differentiation of encephalitogenic Th17 cells.
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