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Regulation and functions of NLRP3 inflammasome during influenza virus infection.

Abstract：

: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.

journal_name

Mol Immunol

journal_title

Molecular immunology

authors

Kuriakose T,Kanneganti TD

doi

10.1016/j.molimm.2017.01.023

subject

Has Abstract

pub_date

2017-06-01 00:00:00

pages

56-64

eissn

0161-5890

issn

1872-9142

pii

S0161-5890(17)30029-9

journal_volume

86

pub_type

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