GADD45γ mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells
GADD45γ mediates the activation of the p38 and JNK MAP kinase pathways and cytokine production in effector TH1 cells
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DOI：
10.1016/s1074-7613(01)00141-8
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发表时间：
2001-05-01
期刊：
影响因子：
32.4
通讯作者：
Flavell, RA
中科院分区：
文献类型：
--
作者：
Lu, BF;Yu, H;Flavell, RA
p38和JNK应激激活的MAPK信号转导途径由T细胞受体（TCR）信号转导激活，并且是T（H）1效应细胞产生IFN-γ所需的。在这里，我们表明GADD 45 γ的表达在T细胞活化过程中被诱导，并且在TH 1细胞中的表达水平高于T（H）2细胞。来自GADD 45 γ（-1-）小鼠的T（H）1细胞在响应TCR信号传导而激活p38和JNK的能力方面严重受损，在再刺激时产生少得多的IFN-γ，并且在激活诱导的细胞死亡（AICD）方面缺乏。此外，GADD 45 γ缺陷导致小鼠接触性超敏反应降低。因此，GADD 45 γ介导p38和JNK通路的活化以及T（H）1细胞的效应子功能。
The p38 and JNK stress-activated MAPK signal transduction pathways are activated by T cell receptor (TCR) signaling and are required for IFN-gamma production by T(H)1 effector cells. Here, we show that the expression of GADD45 gamma is induced during T cell activation and that the level of expression is higher in TH1 cells than in T(H)2 cells. T(H)1 cells from GADD45 gamma (-1-) mice are severely compromised in their abilities to activate p38 and JNK in response to TCR signaling, produce much less IFN-gamma upon restimulation, and are deficient in activation-induced cell death (AICD). Additionally, GADD45 gamma deficiencies caused reduced contact hypersensitivity in mice. Thus, GADD45 gamma mediates activation of the p38 and JNK pathways and effector function of T(H)1 cells.