Defective T cell differentiation in the absence of Jnk1
Defective T cell differentiation in the absence of Jnk1
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DOI：
10.1126/science.282.5396.2092
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发表时间：
1998-12-11
期刊：
影响因子：
56.9
通讯作者：
Flavell, RA
中科院分区：
文献类型：
--
作者：
Dong, C;Yang, DD;Flavell, RA
c-Jun NH 2-末端激酶（JNK）信号传导途径与由CD 4辅助T（T-H）细胞活化和分化为T（H）1和T（H）2效应细胞介导的免疫应答有关。在野生型活化的T-H细胞中观察到的JNK活性在来自Jnk 1（-/-）小鼠的T-H细胞中严重降低。Jnk 1（-/-）T细胞过度增殖，表现出减少的活化诱导的细胞死亡，并优先分化为T（H）2细胞。JNK 1（-/-）细胞产生T（H）2细胞因子的增强与转录因子NFATc的核积累增加有关。因此，JNK 1信号通路在T细胞受体启动的T-H细胞增殖、凋亡和分化中起关键作用。
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 (T-H) cells into T(H)1 and T(H)2 effector cells. JNK activity observed in wild-type activated T-H cells was severely reduced in T-H cells from Jnk1(-/-) mice. The Jnk1(-/-) T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to T(H)2 cells. The enhanced production of T(H)2 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 T-H cell proliferation, apoptosis, and differentiation.