Critical roles of c-Rel in autoimmune inflammation and helper T cell differentiation
Critical roles of c-Rel in autoimmune inflammation and helper T cell differentiation
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DOI：
10.1172/jci200215254
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发表时间：
2002-09-01
影响因子：
15.9
通讯作者：
Chen, YH
中科院分区：
文献类型：
--
作者：
Hilliard, BA;Mason, N;Chen, YH
Rel/NF-kappaB家族的不同成员可能在免疫和炎症中发挥不同的作用。我们在这里报道，c-rel缺陷小鼠对自身免疫性脑脊髓炎具有抵抗力，并且Th1反应有缺陷，但Th2反应不存在。Th1缺陷似乎是由于c-Rel缺陷的抗原提呈细胞选择性地阻断IL-12的产生，以及c-Rel缺陷的T细胞中干扰素-γ的表达完全取消所致。有趣的是，c-rel缺乏并不影响T-bet的表达，提示c-rel可能在Th1细胞分化过程中作用于T-bet下游。因此，与选择性调节Th2细胞分化的核因子-kappaB1不同，c-Rel对Th1细胞分化和Th1细胞介导的自身免疫性炎症是必不可少的。
Different members of the Rel/NF-kappaB 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-gamma 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-kappaB1, which selectively regulates Th2 cell differentiation, c-Rel is essential for Th1 cell differentiation and Th1 cell-mediated autoimmune inflammation.