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

Y Yang, J Weiner, Y Liu, AJ Smith, DJ Huss… - Journal of Experimental …, 2009 - rupress.org
Y Yang, J Weiner, Y Liu, AJ Smith, DJ Huss, R Winger, H Peng, PD Cravens, MK Racke
Journal of Experimental Medicine, 2009rupress.org
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)-1β, IL-6, and IL-23 with transforming growth factor β 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 …
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)-1β, IL-6, and IL-23 with transforming growth factor β 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 γ and IL-17.
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