Regulation and functions of NLRP3 inflammasome during influenza virus infection

被引:62
作者
Kuriakose, Teneema [1 ]
Kanneganti, Thirumala-Devi [1 ]
机构
[1] St Jude Childrens Res Hosp, Dept Immunol, MS 351,262 Danny Thomas Pl, Memphis, TN 38105 USA
基金
美国国家卫生研究院;
关键词
NLRP3; Caspase-1; Inflammasome; Influenza virus; ZBPI; RIPK3; ADAPTIVE IMMUNE-RESPONSES; SINGLE-STRANDED RNA; NF-KAPPA-B; A VIRUS; NS1; PROTEIN; GASDERMIN D; HUMAN MACROPHAGES; VIRAL-INFECTION; INNATE IMMUNITY; CELL-DEATH;
D O I
10.1016/j.molimm.2017.01.023
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The NLRP3 inflammasome constitutes a major antiviral host defense mechanism during influenza virus infection. Inflammasome assembly in virus-infected cells facilitates autocatalytic processing of procaspase-1 and subsequent cleavage and secretion of proinflammatory cytokines IL-1 beta 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. (c) 2017 Elsevier Ltd. All rights reserved.
引用
收藏
页码:56 / 64
页数:9
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