Yu Junyang, Wu Yuzhang, Wang Jingxue
Institute of Immunology, Third Military Medical University, Chongqing, China.
Front Immunol. 2017 Oct 31;8:1420. doi: 10.3389/fimmu.2017.01420. eCollection 2017.
NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome activation and effects during ribonucleic acid (RNA) viral infection are the focus of a wide range of research currently. Both the pathogen-associated molecule pattern derived from virions and intracellular stress molecules involved in the process of viral infection lead to activation of the NLRP3 inflammasome, which in turn triggers inflammatory responses for antiviral defense and tissue healing. However, aberrant activation of the NLRP3 inflammasome can instead support viral pathogenesis and promote disease progression. Here, we summarize and expound upon the recent literature describing the molecular mechanisms underlying the activation and effects of the NLRP3 inflammasome in RNA viral infection to highlight how it provides protection against RNA viral infection.
含NACHT、LRR和PYD结构域蛋白3(NLRP3)炎性小体在核糖核酸(RNA)病毒感染过程中的激活及作用是目前众多研究的焦点。源自病毒粒子的病原体相关分子模式以及参与病毒感染过程的细胞内应激分子均可导致NLRP3炎性小体的激活,进而引发炎症反应以进行抗病毒防御和组织修复。然而,NLRP3炎性小体的异常激活反而可能支持病毒发病机制并促进疾病进展。在此,我们总结并阐述了近期有关NLRP3炎性小体在RNA病毒感染中激活及作用的分子机制的文献,以突出其如何提供针对RNA病毒感染的保护作用。