病毒与宿主的“博弈”:炎性小体的激活与调控

Interaction between virus and host:activation and regulation of inflammasomes

炎性小体是一种由多蛋白质构成的复合结构,可对特定病原体、环境刺激和宿主细胞损伤产生免疫反应。炎性小体通过引起半胱氨酸蛋白水解酶-1(caspase-1)自我剪切、活化,进而裂解白介素-1β前体(pro-IL-1β)和白介素-18前体(pro-IL-18),形成成熟的白介素-1β(IL-1β)和白介素-18(IL-18)。活化的caspase-1也能裂解Gasdermin D蛋白(GSDMD),从而导致一种特殊的细胞死亡,称为细胞焦亡。不同的病毒感染宿主细胞后会激活相应的炎性小体,使机体抵御病毒等病原体感染。本文讨论了炎性小体在病毒感染中的重要性以及病毒为逃避炎性小体依赖性免疫应答而进化出的逃避策略。

Inflammasomes are a complex composed of a variety of proteins,which can produce immune responses to specific pathogens,environmental stimulation and host cell damage.Inflammasomes can induce the activation of caspase-1,cleavage of pro-IL-1βand pro-IL-18 and secretion of corresponding mature cytokines IL-1βand IL-18.Activated caspase-1 can also cleave Gasdermin D,resulting in a special type of cell death called cell pyrolysis.After different viruses infect host cells,they will activate the corresponding inflammasomes and make the body resist the infection of viruses and other pathogens.In this review,we discussed the importance of inflammasomes in viral infection and the escape strategies that viruses have evolved to evade the immune response dependent on inflammasomes.