首页> 外文期刊>The Journal of Infectious Diseases >Human Peripheral gamma delta T Cells Potentiate the Early Proinflammatory Cytokine Response to Staphylococcal Toxic Shock Syndrome Toxin-1.
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Human Peripheral gamma delta T Cells Potentiate the Early Proinflammatory Cytokine Response to Staphylococcal Toxic Shock Syndrome Toxin-1.

机译:人外周γT细胞增强对葡萄球菌毒性休克综合征毒素-1的早期促炎细胞因子反应。

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摘要

Toxic shock syndrome toxin (TSST)-1 is a superantigen known to profoundly induce proinflammatory cytokines by activation of V beta -specific alpha beta T cells, but its effect on gamma delta T cells, which normally constitute 1%-5% of peripheral blood mononuclear cells (PBMCs), is unclear. Here, we demonstrate that TSST-1 induced significantly higher levels of interferon (IFN)- gamma, tumor necrosis factor (TNF)- alpha, and interleukin (IL)-2, and a lower level of IL-10 in human PBMCs when the gamma delta subpopulation has been primed by isopentylpyrophosphate, compared with that in control PBMCs. Furthermore, depletion of the gamma delta subpopulation completely abrogated this effect. Thus, peripheral gamma delta T cells markedly modulate both the proinflammatory and anti-inflammatory cytokine responses of TSST-1.
机译:毒性休克综合征毒素(TSST)-1是一种超抗原,已知会通过激活Vβ特异性αβT细胞深刻诱导促炎性细胞因子,但对通常构成外周血1%-5%的γ-δT细胞有影响单核细胞(PBMC),尚不清楚。在这里,我们证明TSST-1诱导人PBMC中干扰素(IFN)-γ,肿瘤坏死因子(TNF)-α和白介素(IL)-2的水平明显升高,而IL-10的水平降低。与对照组PBMC相比,γ-δ亚群已经被焦磷酸异戊基引发。此外,γ-δ亚群的耗尽完全消除了这种影响。因此,外周γδT细胞显着调节TSST-1的促炎和抗炎细胞因子反应。

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