Cell Biology Assays Team, Biomedical Manufacturing, Commonwealth Scientific and Industrial Research Organisation (CSIRO), Clayton, VIC, Australia.
Centre for Inflammatory diseases, Department of Medicine, School of Clinical Sciences at Monash Health, Monash University, Clayton, VIC, Australia.
Front Immunol. 2022 Aug 30;13:987453. doi: 10.3389/fimmu.2022.987453. eCollection 2022.
The innate immune response to viruses is critical for the correct establishment of protective adaptive immunity. Amongst the many pathways involved, the NLRP3 [nucleotide-binding oligomerisation domain (NOD)-like receptor protein 3 (NLRP3)] inflammasome has received considerable attention, particularly in the context of immunity and pathogenesis during infection with influenza A (IAV) and SARS-CoV-2, the causative agent of COVID-19. Activation of the NLRP3 inflammasome results in the secretion of the proinflammatory cytokines IL-1β and IL-18, commonly coupled with pyroptotic cell death. While this mechanism is protective and key to host defense, aberrant NLRP3 inflammasome activation causes a hyperinflammatory response and excessive release of cytokines, both locally and systemically. Here, we discuss key molecules in the NLRP3 pathway that have also been shown to have significant roles in innate and adaptive immunity to viruses, including DEAD box helicase X-linked (DDX3X), vimentin and macrophage migration inhibitory factor (MIF). We also discuss the clinical opportunities to suppress NLRP3-mediated inflammation and reduce disease severity.
先天免疫反应对于病毒的正确建立保护性适应性免疫至关重要。在涉及的许多途径中,NLRP3 [核苷酸结合寡聚化结构域(NOD)样受体蛋白 3(NLRP3)] 炎性小体受到了相当多的关注,特别是在感染甲型流感(IAV)和 SARS-CoV-2(COVID-19 的致病因子)期间的免疫和发病机制方面。NLRP3 炎性小体的激活导致促炎细胞因子 IL-1β 和 IL-18 的分泌,通常与细胞焦亡死亡相关。虽然这种机制具有保护作用,是宿主防御的关键,但 NLRP3 炎性小体的异常激活会导致局部和全身过度释放细胞因子,引起过度的炎症反应。在这里,我们讨论了 NLRP3 途径中的关键分子,这些分子也被证明在病毒的先天和适应性免疫中具有重要作用,包括 DEAD 盒解旋酶 X 连锁(DDX3X)、波形蛋白和巨噬细胞移动抑制因子(MIF)。我们还讨论了抑制 NLRP3 介导的炎症和降低疾病严重程度的临床机会。