病毒感染激活和抑制炎症小体的研究进展

Research Progress in Activation and Inhibition of Inflammasome by Viral Infection

促炎细胞因子白细胞介素1β(IL-1β)和白细胞介素18(IL-18)主要由巨噬细胞和树突细胞产生,是宿主针对各种侵入病原体产生先天免疫应答的重要介质。这些促炎细胞因子从病毒感染的细胞中分泌,被称为炎症小体的多蛋白复合物严格调控。根据炎症小体识别蛋白的种类,炎症小体主要分为两类,即核苷酸结合寡聚结构域样受体(NOD-like receptors,NLRs)和黑色素瘤缺乏因子2样受体(Absent in melanoma 2,AIM2)炎症小体。与其他宿主防御机制不同,炎症小体活化后,会诱导促炎细胞因子IL-1β、IL-18的成熟及分泌。适量的促炎细胞因子有利于控制病理性感染,但如果过量,则会对机体造成一定免疫损伤。本文主要对近几年有关病毒感染对炎症小体的激活和抑制机制进行了综述,总结分析了炎症小体在参与天然免疫反应及病毒感染致病过程中具有的重要作用。

The pro-inflammatory cytokines interleukin(IL)-1βand IL-18 are produced primarily by macrophages and dendritic cells,and are important mediators in innate immune responses against various invading pathogens.Secretion of pro-IL-1βand IL-18 from cells infected with pathogens is tightly regulated by large cytosolic multiprotein complexes called"inflammasomes".The inflammasome can be classified as nucleotide-binding oligomerization domain-like receptors(NLRs)inflammasome and absent in melanoma 2-1 ike receptor(AIM2)inflammasome according to the types of receptors that recognize inflammatory signal.Unlike other host defense mechanisms,inflammasome activation can induce the maturation and secretion of pro-IL-1βand pro-IL-18.Although appropriate amounts of pro-inflammatory cytokines are beneficial for controlling pathogenic infections,excessive levels of pro-inflammatory cytokines can cause damage to the immune system.This review focuses on the research progress in activation and inhibition of inflammasome by viral infection,and summarizes the importance of inflammasome in innate immune responses and viral infection.