Toll样受体4介导慢性束缚应激诱导的免疫抑制。
Toll-like receptor 4 mediates chronic restraint stress-induced immune suppression.
作者信息
Zhang Yi, Woodruff Michael, Zhang Ying, Miao Junying, Hanley Gregory, Stuart Charles, Zeng Xiao, Prabhakar Savita, Moorman Jonathan, Zhao Baoxiang, Yin Deling
机构信息
Departments of Internal Medicine, James Quillen College of Medicine, East Tennessee State University, Johnson City, TN 37614, United States.
出版信息
J Neuroimmunol. 2008 Feb;194(1-2):115-22. doi: 10.1016/j.jneuroim.2007.12.002. Epub 2008 Jan 14.
Abstract
Stress, either physical or psychological, can have a dramatic impact on the immune system. Little progress, however, has been made in understanding stress-induced immune suppression. We report here that mice subjected to chronic 12-hour daily physical restraint for two days significantly increased the expression of Toll-like receptor 4 (TLR4). Interestingly, TLR4-deficient mice are resistant to stress-induced lymphocyte reduction. In addition, restraint stress caused dramatic decrease in T help 1 (Th1) cytokine IFN-gamma and IL-2 levels but increase in Th2 cytokine IL-4 in wild type mice. Moreover, the restraint stress significantly inhibits changes of Th1 and Th2 cytokines in TLR4-deficient mice compared with the wild type mice. Therefore, stress modulates the immune system through a TLR4-dependent mechanism.
摘要
身体或心理上的压力都可能对免疫系统产生巨大影响。然而，在理解压力诱导的免疫抑制方面进展甚微。我们在此报告，每天接受12小时慢性身体束缚两天的小鼠，其Toll样受体4（TLR4）的表达显著增加。有趣的是，TLR4缺陷型小鼠对压力诱导的淋巴细胞减少具有抗性。此外，在野生型小鼠中，束缚压力导致辅助性T细胞1（Th1）细胞因子IFN-γ和IL-2水平显著降低，但Th2细胞因子IL-4水平升高。而且，与野生型小鼠相比，束缚压力显著抑制了TLR4缺陷型小鼠中Th1和Th2细胞因子的变化。因此，压力通过一种依赖TLR4的机制调节免疫系统。
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