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An update on cell intrinsic negative regulators of the NLRP3 inflammasome
Author(s) -
Poudel Barun,
Gurung Prajwal
Publication year - 2018
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.3mir0917-350r
Subject(s) - inflammasome , pyroptosis , inflammation , biology , programmed cell death , microbiology and biotechnology , cytokine storm , aim2 , caspase 1 , innate immune system , immune system , cytokine , immunology , apoptosis , medicine , disease , biochemistry , covid-19 , pathology , infectious disease (medical specialty)
Inflammasomes are multimeric protein complexes that promote inflammation (through specific cleavage and production of bioactive IL‐1β and IL‐18) and pyroptotic cell death. The central role of inflammasomes in combating infection and maintaining homeostasis has been studied extensively. Although inflammasome‐mediated inflammation and cell death are vital to limit pathogenic insults and to promote wound healing/tissue regeneration, unchecked/uncontrolled inflammation, and cell death can cause cytokine storm, tissue damage, autoinflammatory and autoimmune diseases, and even death in the afflicted individuals. NLRP3 is one of the major cytosolic sensors that assemble an inflammasome. Given the adverse consequences of uncontrolled inflammasome activation, our immune system has developed tiered mechanisms to inhibit NLRP3 inflammasome activation. In this review, we highlight and discuss recent advances and our current understanding of mechanisms by which NLRP3 inflammasome can be negatively regulated.