Regulation and functions of NLRP3 inflammasome during influenza virus infection


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Abstract

HighlightsThe NLRP3 inflammasome promotes host protective responses during influenza virus infection.Host factors regulating inflammasome activation include TLR and RIG-I sensors and type I IFN signaling.The IFN-inducible protein ZBP1 functions as a common upstream regulator of NLRP3 inflammasome and programmed cell death pathways during influenza virus infection.Virus encoded proteins NS1, M2 and PB1-F2 facilitate inflammasome activation.The NLRP3 inflammasome constitutes a major antiviral host defense mechanism during influenza virus infection. Inflammasome assembly in virus-infected cells facilitates autocatalytic processing of pro-caspase-1 and subsequent cleavage and secretion of proinflammatory cytokines IL-1β and IL-18. The NLRP3 inflammasome is critical for induction of both innate and adaptive immune responses during influenza virus infection. Inflammasome-dependent antiviral responses also regulate immunopathology and tissue repair in the infected lungs. The regulation of NLRP3 inflammasome assembly is an area of active research and recent studies have unraveled multiple cellular and viral factors involved in inflammasome assembly. Emerging studies have also identified the cross talk between inflammasome activation and programmed cell death pathways in influenza virus-infected cells. Here, we review the current literature regarding regulation and functions of NLRP3 inflammasome during influenza virus infection.

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