Dong C, Yang D D, Wysk M, Whitmarsh A J, Davis R J, Flavell R A
Section of Immunobiology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA.
Science. 1998 Dec 11;282(5396):2092-5. doi: 10.1126/science.282.5396.2092.
The c-Jun NH2-terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice. The Jnk1-/- T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to TH2 cells. The enhanced production of TH2 cytokines by Jnk1-/- cells was associated with increased nuclear accumulation of the transcription factor NFATc. Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation.
c-Jun氨基末端激酶（JNK）信号通路参与了由CD4辅助性T（TH）细胞激活并分化为TH1和TH2效应细胞所介导的免疫反应。在野生型活化TH细胞中观察到的JNK活性在Jnk1-/-小鼠的TH细胞中严重降低。Jnk1-/- T细胞过度增殖，活化诱导的细胞死亡减少，并优先分化为TH2细胞。Jnk1-/-细胞增强的TH2细胞因子产生与转录因子NFATc的核内积累增加有关。因此，JNK1信号通路在T细胞受体启动的TH细胞增殖、凋亡和分化中起关键作用。
