IRF3 和 ERK MAP 激酶控制巨噬细胞对 poly-I:C 的反应中一氧化氮的产生。
IRF3 and ERK MAP-kinases control nitric oxide production from macrophages in response to poly-I:C.
机构信息
School of Biological Sciences, University of Nebraska-Lincoln, Lincoln, NE, USA.
出版信息
FEBS Lett. 2013 Sep 17;587(18):3014-20. doi: 10.1016/j.febslet.2013.07.025. Epub 2013 Jul 23.
Abstract
Understanding nitric oxide (NO) in innate anti-viral immunity and immune-mediated pathology is hampered by incomplete details of its transcriptional and signaling factors. We found in macrophages that IRF3, ERK MAP-kinases, and PKR are essential to NO production in response to RNA-virus mimic, poly I:C, a TLR3 agonist. ERK's role in NO induction may be through phosphorylation of serine-171 of IRF3 and expression of NO-inducing cytokines, IL-6 and IFN-β. However, these cytokines induced less NO in IRF3 knockout or knockdown macrophages. These findings show that ERK and IRF3 coordinate induction of NO by macrophages in response to stimulation of TLR3.
摘要
理解先天抗病毒免疫和免疫介导的病理生理学中的一氧化氮（NO）受到其转录和信号因子细节不完整的阻碍。我们在巨噬细胞中发现，IRF3、ERK MAP 激酶和 PKR 对于 RNA 病毒模拟物聚肌苷酸：聚胞苷酸（TLR3 激动剂）诱导的 NO 产生至关重要。ERK 在诱导 NO 中的作用可能是通过磷酸化 IRF3 的丝氨酸 171 和表达诱导 NO 的细胞因子，IL-6 和 IFN-β。然而，这些细胞因子在 IRF3 敲除或敲低巨噬细胞中诱导的 NO 较少。这些发现表明，ERK 和 IRF3 在 TLR3 刺激下协调诱导巨噬细胞产生 NO。
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