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首页> 外文期刊>Cellular immunology >IL-10 induces an immune repressor pathway in sepsis by promoting S100A9 nuclear localization and MDSC development
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IL-10 induces an immune repressor pathway in sepsis by promoting S100A9 nuclear localization and MDSC development

机译：IL-10通过促进S100A9核定位和MDSC发育，诱导败血症的免疫力压抑途径

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摘要

The myeloid-related protein S100A9 reprograms Gr1+CD11b+myeloid precursors into myeloid-derived suppressor cells (MDSCs) during murine sepsis. Here, we show that the immunosuppressive cytokine IL-10 supports S100A9 expression and its nuclear localization in MDSCs to function as immune repressors. To support this new concept, we showed that antibody mediated IL-10 blockade in wild-type mice after sepsis induction inhibited MDSC expansion during late sepsis, and that ectopic expression of S100A9 in Gr1+CD11b+cells from S100A9 knockout mice switched them into the MDSC phenotype only in the presence of IL-10. Knockdown of S100A9 in MDSCs from wild-type mice with late sepsis confirmed our findings in the S100A9 knockout mice. We also found that while both IL-6 and IL-10 can activate S100A9 expression in naive Gr1+CD11b+cells, only IL-10 can induce S100A9 nuclear localization. These results support that IL-10 drives the molecular path that generates MDSCs and enhances immunosuppression during late sepsis, and inform that targeting this immune repressor path may improve sepsis survival in mice.
机译：粘虫相关蛋白S100A9在鼠脓毒症期间重新编程GR1 + CD11b +髓样前体（MDSCS）尿素衍生的抑制细胞（MDSC）。在这里，我们表明免疫抑制细胞因子IL-10支持S100A9表达及其在MDSC中的核定位，以用作免疫压抑。为了支持这种新概念，我们展示患者在败血症诱导期间抑制MDSC膨胀后的野生型小鼠的抗体介导的IL-10阻断，并且来自S100A9敲除小鼠的GR1 + CD11b +细胞的S100a9中的异位表达切换到MDSC表型仅在IL-10存在下。来自败血症晚期野生型小鼠的MDSC中的S100A9敲低证实了我们在S100A9敲除小鼠中的发现。我们还发现，虽然IL-6和IL-10可以在幼稚GR1 + CD11b +细胞中激活S100A9表达，但只有IL-10可以诱导S100A9核定位。这些结果支持IL-10驱动产生MDSC的分子径，并在后期败血症期间增强免疫抑制，并告知靶向这种免疫压缩路径可以改善小鼠中的脓毒症生存率。

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