T-bet is essential for encephalitogenicity of both Th1 and Th17 cells Export

@article{citeulike:4932766, abstract = {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)-1{beta}, 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. 10.1084/jem.20082584}, author = {Yang, Yuhong and Weiner, Jeffrey and Liu, Yue and Smith, Alan J. and Huss, David J. and Winger, Ryan and Peng, Haiyan and Cravens, Petra D. and Racke, Michael K. and Lovett-Racke, Amy E.}, citeulike-article-id = {4932766}, citeulike-linkout-0 = {http://dx.doi.org/10.1084/jem.20082584}, day = {22}, doi = {10.1084/jem.20082584}, journal = {J. Exp. Med.}, keywords = {autoimmune\_diseases, eae, immune\_regulation, t-bet, t\_cells, t\_helper\_cells, th17\_cells, th1\_cells}, month = {June}, pages = {jem.20082584+}, posted-at = {2009-06-23 11:59:48}, priority = {2}, title = {T-bet is essential for encephalitogenicity of both Th1 and Th17 cells}, url = {http://dx.doi.org/10.1084/jem.20082584}, year = {2009} }

TY - JOUR ID - citeulike:4932766 L3 - citeulike-article-id:4932766 N2 - 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)-1{beta}, 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. 10.1084/jem.20082584 JF - J. Exp. Med. TI - T-bet is essential for encephalitogenicity of both Th1 and Th17 cells SP - jem.20082584 KW - autoimmune_diseases KW - eae KW - immune_regulation KW - t-bet KW - t_cells KW - t_helper_cells KW - th17_cells KW - th1_cells AU - Yang, Yuhong AU - Weiner, Jeffrey AU - Liu, Yue AU - Smith, Alan AU - Huss, David AU - Winger, Ryan AU - Peng, Haiyan AU - Cravens, Petra AU - Racke, Michael AU - Lovett-Racke, Amy PY - 2009/06/22/ UR - http://dx.doi.org/10.1084/jem.20082584 ER -