MaruYama Takashi
Laboratory of Cell Recognition and Response, Graduate School of Life Sciences, Tohoku University, Sendai, Miyagi 980-8578, Japan; School of Medicine, Gifu University, Gifu 501-1194, Japan.
Biochem Biophys Res Commun. 2015 Aug 21;464(2):586-9. doi: 10.1016/j.bbrc.2015.07.013. Epub 2015 Jul 7.
Inhibitor of kappa B (IκB)-ζ, a member of the nuclear IκB family of proteins, is induced by the transforming growth factor (TGF)-β signaling pathway and plays a pivotal role in maintaining the balance of T helper (Th) cell subsets. IκB-ζ deficiency results in reduced percentages of Th17 cells and increased percentages of Th1 cells. In this study, the effects of IκB-ζ deficiency on T-cell subsets were examined further. The data showed that IκB-ζ-deficient T cells had a high capacity for generation of regulatory T cells (Tregs) when T cells were cultured under TGF-β stimulation in the presence of cytokine-neutralizing antibodies. Mechanistically, IκB-ζ itself negatively regulated activation of the Foxp3 promoter in a nuclear factor of kappaB-dependent manner. Thus, this study showed that IκB-ζ controlled Treg differentiation.
κB抑制蛋白（IκB）-ζ是细胞核IκB蛋白家族的成员之一，由转化生长因子（TGF）-β信号通路诱导产生，并在维持辅助性T（Th）细胞亚群平衡中起关键作用。IκB-ζ缺陷导致Th17细胞百分比降低，Th1细胞百分比增加。在本研究中，进一步检测了IκB-ζ缺陷对T细胞亚群的影响。数据显示，当T细胞在细胞因子中和抗体存在的情况下于TGF-β刺激下培养时，IκB-ζ缺陷的T细胞具有较高的生成调节性T细胞（Tregs）的能力。从机制上讲，IκB-ζ本身以κB依赖的方式对Foxp3启动子的激活进行负调控。因此，本研究表明IκB-ζ控制Treg分化。
