Recent Insights on Inflammasomes, Gasdermin Pores, and Pyroptosis
Author(s) -
Nathalia Moraes de Vasconcelos,
Mohamed Lamkanfi
Publication year - 2019
Publication title -
cold spring harbor perspectives in biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.011
H-Index - 173
ISSN - 1943-0264
DOI - 10.1101/cshperspect.a036392
Subject(s) - pyroptosis , inflammasome , biology , effector , microbiology and biotechnology , aim2 , caspase , caspase 1 , programmed cell death , secretion , innate immune system , inflammation , immune system , apoptosis , immunology , genetics , biochemistry
Inflammasomes assemble in the cytosol of myeloid and epithelial cells on sensing of cellular stress and pathogen-associated molecular patterns and serve as scaffolds for recruitment and activation of inflammatory caspases. Inflammasomes play beneficial roles in host and immune responses against diverse pathogens but may also promote inflammatory tissue damage if uncontrolled. Gasdermin D (GSDMD) is a recently identified substrate of murine caspase-1 and caspase-11, and human caspases-1, -4, and -5 that mediates a regulated lytic cell death mode termed pyroptosis. Recent studies have identified pyroptosis as a critical inflammasome effector mechanism that controls inflammasome-dependent cytokine secretion and contributes to antimicrobial defense and inflammasome-mediated autoinflammatory diseases. Here, we review recent developments on inflammasome-associated effector functions with an emphasis on the emerging roles of gasdermin pores and pyroptosis.
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