CD8(+) T cells promote cytokine responses to stress.
CD8(+) T cells promote cytokine responses to stress.
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DOI：
10.1016/j.cyto.2018.07.015
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发表时间：
2019-01
期刊：
影响因子：
3.8
通讯作者：
Tonelli LH
中科院分区：
文献类型：
--
作者：
Clark SM;Song C;Li X;Keegan AD;Tonelli LH
众所周知，心理压力对免疫功能有深远的影响，并会促进炎症。已知与压力相关的细胞因子循环水平升高会增加患几种疾病的风险，但对其机制知之甚少。本研究评估了习得性无助范式中应激后T细胞对细胞因子水平的影响。CD4+ T细胞过继转染Rag2−/−小鼠后，细胞因子水平对应激没有改变，而CD8+ T细胞导致应激Rag2−/−小鼠中TNF-α、IL-6和IFN-γ水平升高。此外，在WT小鼠中，CD8+ T细胞的消耗消除了这些细胞因子对应激的反应。CD8+ T细胞重组Rag2−/−小鼠皮质酮和行为应激反应性受损。值得注意的是，在WT小鼠中，这些细胞的消耗对行为或皮质酮水平没有影响。应激并没有改变T细胞活化的典型标志物CD62L和CD44的表达，也没有改变细胞内细胞因子的含量，这表明它们不是应激反应中循环细胞因子的主要产生者。这些结果表明，CD8+ T细胞可能通过刺激非淋巴样细胞来促进TNF-α、IL-6和IFN-γ对应激的反应。
Psychological stress is known to have profound effects on immune function and to promote inflammatory conditions. Elevated circulating levels of cytokines associated with stress are known to increase the risk to several diseases, but little is known about this mechanism. This study assessed the role of T cells on cytokine levels after exposure to stress in the learned helplessness paradigm. Adoptive transfer of CD4+ T cells into Rag2−/− mice did not change cytokine levels to stress while CD8+ T cells resulted in an increase in TNF-α, IL-6 and IFN-γ in stressed Rag2−/− mice. Moreover, depletion of CD8+ T cells in WT mice abolished these cytokine responses to stress. Corticosterone and behavioral stress responsiveness was impaired in Rag2−/− mice reconstituted with CD8+ T cells. Notably, depletion of these cells in WT mice had no effect on behavior or corticosterone levels. Exposure to stress did not change the expression of canonical markers of T cell activation including CD62L and CD44 or modified intracellular cytokine content, suggesting that they are not the main producers of circulating cytokines in response to stress. These results show that CD8+ T cells promote TNF-α, IL-6 and IFN-γ responses to stress, possibly by stimulating non-lymphoid cells.
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影响因子：
11
作者：
McKim DB;Weber MD;Niraula A;Sawicki CM;Liu X;Jarrett BL;Ramirez-Chan K;Wang Y;Roeth RM;Sucaldito AD;Sobol CG;Quan N;Sheridan JF;Godbout JP
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通讯作者：
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通讯作者：
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