TGF-β-induced IκB-ζ controls Foxp3 gene expression
TGF-β-induced IκB-ζ controls Foxp3 gene expression
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DOI：
10.1016/j.bbrc.2015.07.013
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发表时间：
2015-08-21
影响因子：
3.1
通讯作者：
MaruYama, Takashi
中科院分区：
文献类型：
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作者：
MaruYama, Takashi
κ B抑制因子（I kappa B）-zeta是细胞核I kappa B家族的成员，由转化生长因子（TGF）-β信号通路诱导，在维持辅助性T细胞（Th）亚群平衡中起关键作用。I κ B-zeta缺乏导致Th 17细胞百分比降低和Th 1细胞百分比增加。在这项研究中，I κ B-zeta缺陷对T细胞亚群的影响进行了进一步研究。数据显示，当T细胞在TGF-β刺激下、在存在精氨酸中和抗体的情况下培养时，I κ B-zeta缺陷型T细胞具有产生调节性T细胞（TcR）的高能力。从机制上讲，I κ B-zeta本身以kappaB依赖性核因子的方式负调节Foxp 3启动子的激活。因此，该研究显示I κ B-zeta控制Treg分化。(C)2015作者爱思唯尔公司出版
Inhibitor of kappa B (I kappa B)-zeta, a member of the nuclear I kappa B family of proteins, is induced by the transforming growth factor (TGF)-beta signaling pathway and plays a pivotal role in maintaining the balance of T helper (Th) cell subsets. I kappa B-zeta deficiency results in reduced percentages of Th17 cells and increased percentages of Th1 cells. In this study, the effects of I kappa B-zeta deficiency on T-cell subsets were examined further. The data showed that I kappa B-zeta-deficient T cells had a high capacity for generation of regulatory T cells (Tregs) when T cells were cultured under TGF-beta stimulation in the presence of cytokine-neutralizing antibodies. Mechanistically, I kappa B-zeta itself negatively regulated activation of the Foxp3 promoter in a nuclear factor of kappaB-dependent manner. Thus, this study showed that I kappa B-zeta controlled Treg differentiation. (C) 2015 The Author. Published by Elsevier Inc.