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Toll-like receptor 9 is required for chronic stress-induced immune suppression

机译:Toll样受体9是慢性应激诱导的免疫抑制所必需的

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摘要

Psychological and physical stress can suppress the immune system in both humans and animals. The mechanism by which stress affects immune responses, however, remains poorly defined. Toll-like receptors (TLRs) play a key role in modulating immune responses and cell survival. The mechanisms by which TLRs modulates chronic stress are largely unexplored. In current study, we revealed that a deficiency of TLR9 is resistant to chronic stress-induced lymphocyte apoptosis. In addition, TLR9 knockout (KO) mice significantly diminish the chronic stress-induced up-regulation of corticosterone levels. Notably, we found that lymphocytes from both TLR9 KO mice and wild type mice were similarly sensitive to corticosteroid-induced cell apoptosis. Moreover, we demonstrated that a deficiency of TLR9 blocks chronic stress-induced imbalance of Th1 and Th2 cytokine levels. Taken together, our findings reveal that TLR9 plays an essential role in chronic stress-induced immune suppression.
机译:心理和生理压力会抑制人类和动物的免疫系统。然而,应激影响免疫反应的机制仍然不清楚。 Toll样受体(TLR)在调节免疫反应和细胞存活中起关键作用。 TLRs调节慢性应激的机制在很大程度上尚待探索。在当前的研究中,我们发现TLR9的缺乏能抵抗慢性应激诱导的淋巴细胞凋亡。此外,TLR9基因敲除(KO)小鼠显着减少了慢性应激诱导的皮质酮水平上调。值得注意的是,我们发现TLR9 KO小鼠和野生型小鼠的淋巴细胞对皮质类固醇诱导的细胞凋亡都同样敏感。此外,我们证明了TLR9的缺乏会阻止慢性应激诱导的Th1和Th2细胞因子水平的失衡。综上所述,我们的发现揭示了TLR9在慢性应激诱导的免疫抑制中起着至关重要的作用。

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