Gadd45 is important for perpetuating cognate and inflammatory signals in T cells
Gadd45 is important for perpetuating cognate and inflammatory signals in T cells
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DOI：
10.1038/ni1020
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发表时间：
2004-01-01
影响因子：
30.5
通讯作者：
Flavell, RA
中科院分区：
文献类型：
--
作者：
Lu, BF;Ferrandino, AF;Flavell, RA
Gadd 45 β（growth arrest and DNA damage-inducible，β）参与细胞周期阻滞、凋亡、信号转导和细胞存活。在T细胞中，Gadd 45 b被T细胞受体（TCR）和炎症信号快速诱导。CD 4（+）T细胞中Gadd 45 β的缺乏损害了它们对TCR刺激或炎性细胞因子的反应。ERK、p38和JNK的激活在Gadd 45 β缺陷型CD 4（+）T细胞中均受到抑制。Gadd 45 β缺陷型CD 4（+）T细胞的细胞因子产生也受到损害。此外，Gadd 45 β介导的树突状细胞的炎性细胞因子的产生，和Gadd 45 β缺陷的小鼠表现出受损的T辅助细胞1型反应在单核细胞增生李斯特菌感染。因此，Gadd 45 β是一个关键的反馈调节因子，使同源信号和炎症信号都持续存在。
Gadd45beta (growth arrest and DNA damage-inducible, beta) is involved in cell cycle arrest, apoptosis, signal transduction and cell survival. In T cells, Gadd45b was rapidly induced by T cell receptor (TCR) and inflammatory signals. Deficiency of Gadd45beta in CD4(+) T cells impaired their responses to TCR stimulation or inflammatory cytokines. ERK, p38 and JNK activation were all substantially suppressed in Gadd45beta-deficient CD4(+) T cells. Cytokine production by Gadd45beta-deficient CD4(+) T cells was also impaired. Furthermore, Gadd45beta mediated inflammatory cytokine production by dendritic cells, and Gadd45beta-deficient mice showed an impaired T helper type 1 response during Listeria monocytogenes infection. Gadd45beta is therefore a critical feedback regulator that perpetuates both cognate and inflammatory signals.