| First Author | Yang Y | Year | 2009 |
| Journal | J Exp Med | Volume | 206 |
| Issue | 7 | Pages | 1549-64 |
| PubMed ID | 19546248 | Mgi Jnum | J:150271 |
| Mgi Id | MGI:3850262 | Doi | 10.1084/jem.20082584 |
| Citation | Yang Y, et al. (2009) T-bet is essential for encephalitogenicity of both Th1 and Th17 cells. J Exp Med 206(7):1549-64 |
| abstractText | The extent to which myelin-specific Th1 and Th17 cells contribute to the pathogenesis of experimental autoimmune encephalomyelitis (EAE) is controversial. Combinations of interleukin (IL)-1beta, IL-6, and IL-23 with transforming growth factor beta were used to differentiate myelin-specific T cell receptor transgenic T cells into Th17 cells, none of which could induce EAE, whereas Th1 cells consistently transferred disease. However, IL-6 was found to promote the differentiation of encephalitogenic Th17 cells. Further analysis of myelin-specific T cells that were encephalitogenic in spontaneous EAE and actively induced EAE demonstrated that T-bet expression was critical for pathogenicity, regardless of cytokine expression by the encephalitogenic T cells. These data suggest that encephalitogenicity of myelin-specific T cells appears to be mediated by a pathway dependent on T-bet and not necessarily pathway-specific end products, such as interferon gamma and IL-17. |
