本文關(guān)鍵詞：細(xì)胞因子風(fēng)暴，由筆耕文化傳播整理發(fā)布。

細(xì)胞因子風(fēng)暴是指免疫細(xì)胞及其活性產(chǎn)物（細(xì)胞因子）過(guò)量生產(chǎn)的現(xiàn)象。在流感病毒感染時(shí)，細(xì)胞因子風(fēng)暴會(huì)導(dǎo)致大量活化的免疫細(xì)胞涌入肺部，而這種情況往往會(huì)提高患者的死亡率。

生物通編輯：葉予

生物通推薦原文摘要：

Mapping the innate signaling cascade essential for cytokine storm during influenza virus infection

During pathogenic influenza virus infection, robust cytokine production (cytokine storm), excessive inflammatory infiltrates, and virus-induced tissue destruction all contribute to morbidity and mortality. Earlier we reported that modulation of sphingosine-1-phosphate-1 receptor (S1P1R) signaling provided a chemically tractable approach for the effective blunting of cytokine storm, leading to the improvement of clinical and survival outcomes. Here, we show that S1P1R agonist treatment suppresses global cytokine amplification. Importantly, S1P1R agonist treatment was able to blunt cytokine/chemokine production and innate immune cell recruitment in the lung independently of endosomal and cytosolic innate sensing pathways. S1P1R signaling suppression of cytokine amplification was independent of multiple innate signaling adaptor pathways for myeloid differentiation primary response gene 88 (MyD88) and IFN-β promoter stimulator-1 signaling, indicating a common pathway inhibition of cytokine storm. We identify the MyD88 adaptor molecule as responsible for the majority of cytokine amplification observed following influenza virus challenge.

  本文關(guān)鍵詞：細(xì)胞因子風(fēng)暴，由筆耕文化傳播整理發(fā)布。