Brendan A. Hilliard, Nicola Mason, Lingyun Xu, Jing Sun, Salah-Eddine Lamhamedi-Cherradi, Hsiou-Chi Liou, Christopher Hunter, Youhai H. Chen
J Clin Invest.
2002;
110(6):843–850
doi:10.1172/JCI15254
This article Copyright © 2002, The American Society for Clinical Investigation
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D
ifferent members of the Rel/NF-κB family may play different roles in immunity and inflammation. We report here that c-Rel–deficient mice are resistant to autoimmune encephalomyelitis and are defective in Th1, but not Th2 responses. The Th1 deficiency appears to be caused by selective blockade of IL-12 production by c-Rel–deficient antigen-presenting cells, as well as by a complete abrogation of IFN-γ expression in c-Rel–deficient T cells. Interestingly, c-Rel deficiency does not affect T-bet expression, suggesting that c-Rel may act downstream of T-bet during Th1 cell differentiation. Thus, unlike NF-κB1, which selectively regulates Th2 cell differentiation, c-Rel is essential for Th1 cell differentiation and Th1 cell–mediated autoimmune inflammation.
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