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首页> 外文期刊>Nature immunology >The kinases MSK1 and MSK2 act as negative regulators of Toll-like receptor signaling.
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The kinases MSK1 and MSK2 act as negative regulators of Toll-like receptor signaling.

机译：激酶MSK1和MSK2充当Toll样受体信号转导的负调节剂。

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摘要

The kinases MSK1 and MSK2 are activated 'downstream' of the p38 and Erk1/2 mitogen-activated protein kinases. Here we found that MSK1 and MSK2 were needed to limit the production of proinflammatory cytokines in response to stimulation of primary macrophages with lipopolysaccharide. By inducing transcription of the mitogen-activated protein kinase phosphatase DUSP1 and the anti-inflammatory cytokine interleukin 10, MSK1 and MSK2 exerted many negative feedback mechanisms. Deficiency in MSK1 and MSK2 prevented the binding of phosphorylated transcription factors CREB and ATF1 to the promoters of the genes encoding interleukin 10 and DUSP1. Mice doubly deficient in MSK1 and MSK2 were hypersensitive to lipopolysaccharide-induced endotoxic shock and showed prolonged inflammation in a model of toxic contact eczema induced by phorbol 12-myristate 13-acetate. Our results establish MSK1 and MSK2 as key components of negative feedback mechanisms needed to limit Toll-like receptor-driven inflammation.
机译：激酶MSK1和MSK2在p38和Erk1 / 2丝裂原激活的蛋白激酶的“下游”被激活。在这里，我们发现需要MSK1和MSK2来限制促炎细胞因子的产生，以响应脂多糖对原代巨噬细胞的刺激。通过诱导有丝分裂原激活的蛋白激酶磷酸酶DUSP1和抗炎细胞因子白介素10的转录，MSK1和MSK2发挥了许多负面反馈机制。 MSK1和MSK2的缺乏阻止了磷酸化的转录因子CREB和ATF1与编码白介素10和DUSP1的基因的启动子结合。双倍缺乏MSK1和MSK2的小鼠对脂多糖诱导的内毒素休克过敏，并在佛波醇12-肉豆蔻酸酯13-乙酸酯诱导的毒性接触性湿疹模型中显示出长时间的炎症。我们的结果将MSK1和MSK2确立为限制Toll样受体驱动的炎症所需的负反馈机制的关键组成部分。

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