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Toll样受体2参与初始CD4+ T细胞通过调节Th1/Th2和Th17来挽救应激诱导的免疫抑制。

TLR2 Involved in Naive CD4+ T Cells Rescues Stress-Induced Immune Suppression by Regulating Th1/Th2 and Th17.

作者信息

Zhao Jing, Liu Jing, Denney James, Li Chen, Li Fang, Chang Fen, Chen Mingyou, Yin Deling

机构信息

Institute of Developmental Biology, School of Life Science, Shandong University, Jinan, China.

出版信息

Neuroimmunomodulation. 2015;22(5):328-36. doi: 10.1159/000371468. Epub 2015 Feb 25.

Abstract

Stress, either physical or psychological, can have a dramatic impact on our immune system. There has been little progress, however, in understanding chronic stress-induced immunosuppression. Naive CD4+ T cells could modulate immune responses via differentiation to T helper (Th) cells. In this study, we showed that stress promotes the release of the Th1 cytokines interferon (IFN)-γ and tumor necrosis factor (TNF)-α, the Th2 cytokines interleukin (IL)-4 and IL-10 and the Th17 cytokine IL-17 of splenic naive CD4+ T cells. This suggests that stress promotes the differentiation of naive CD4+ T cells to Th1, Th2 and Th17 cells. Knockout strategies verified that TLR2 might modulate the differentiation of Th1/Th2 cells by inhibiting p38 mitogen-activated protein kinase (MAPK). Taken together, our data suggest that chronic stress induces immune suppression by targeting TLR2 and p38 MAPK in naive CD4+ T cells.

摘要

身体或心理上的压力都会对我们的免疫系统产生巨大影响。然而,在理解慢性应激诱导的免疫抑制方面进展甚微。初始CD4+ T细胞可通过分化为辅助性T(Th)细胞来调节免疫反应。在本研究中,我们发现应激促进脾脏初始CD4+ T细胞释放Th1细胞因子干扰素(IFN)-γ和肿瘤坏死因子(TNF)-α、Th2细胞因子白细胞介素(IL)-4和IL-10以及Th17细胞因子IL-17。这表明应激促进初始CD4+ T细胞向Th1、Th2和Th17细胞分化。基因敲除策略证实,Toll样受体2(TLR2)可能通过抑制p38丝裂原活化蛋白激酶(MAPK)来调节Th1/Th2细胞的分化。综上所述,我们的数据表明,慢性应激通过靶向初始CD4+ T细胞中的TLR2和p38 MAPK诱导免疫抑制。

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