| First Author | Duhen R | Year | 2013 |
| Journal | J Immunol | Volume | 190 |
| Issue | 9 | Pages | 4478-82 |
| PubMed ID | 23543757 | Mgi Jnum | J:195506 |
| Mgi Id | MGI:5484699 | Doi | 10.4049/jimmunol.1203172 |
| Citation | Duhen R, et al. (2013) Cutting Edge: The Pathogenicity of IFN-gamma-Producing Th17 Cells Is Independent of T-bet. J Immunol 190(9):4478-82 |
| abstractText | During the development of experimental autoimmune encephalomyelitis (EAE), the proportion of pathogenic and myelin-specific cells within CNS-infiltrating cytokine-producing Th cells is unknown. Using an IL-17A/IFN-gamma double reporter mouse and I-A(b)/myelin oligodendrocyte glycoprotein 38-49 tetramer, we show in this study that IL-17(+)IFN-gamma(+) Th cells, which are expanded in the CNS during EAE, are highly enriched in myelin oligodendrocyte glycoprotein-specific T cells. We further demonstrate that IL-23 is essential for the generation and expansion of IFN-gamma-producing Th17 cells independently of the Th1-associated transcription factors T-bet, STAT1, and STAT4. Furthermore, Th17 and IL-17(+)IFN-gamma(+) Th cells can induce CNS autoimmunity independently of T-bet. Whereas T-bet is crucial for Th1-mediated EAE, it is dispensable for Th17 cell-mediated autoimmunity. Our results suggest the existence of different epigenetic programs that regulate IFN-gamma expression in Th1 and Th17 cells. |
