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Pyroptotic cell death defends against intracellular pathogens
Author(s) -
Jorgensen Ine,
Miao Edward A.
Publication year - 2015
Publication title -
immunological reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.839
H-Index - 223
eISSN - 1600-065X
pISSN - 0105-2896
DOI - 10.1111/imr.12287
Subject(s) - pyroptosis , inflammasome , biology , caspase 1 , microbiology and biotechnology , programmed cell death , phagocytosis , caspase , innate immune system , lytic cycle , immunology , phagocyte , intracellular , secretion , inflammation , apoptosis , immune system , biochemistry , virus
Summary Inflammatory caspases play a central role in innate immunity by responding to cytosolic signals and initiating a twofold response. First, caspase‐1 induces the activation and secretion of the two prominent pro‐inflammatory cytokines, interleukin‐1β ( IL ‐1β) and IL ‐18. Second, either caspase‐1 or caspase‐11 can trigger a form of lytic, programmed cell death called pyroptosis. Pyroptosis operates to remove the replication niche of intracellular pathogens, making them susceptible to phagocytosis and killing by a secondary phagocyte. However, aberrant, systemic activation of pyroptosis in vivo may contribute to sepsis. Emphasizing the efficiency of inflammasome detection of microbial infections, many pathogens have evolved to avoid or subvert pyroptosis. This review focuses on molecular and morphological characteristics of pyroptosis and the individual inflammasomes and their contribution to defense against infection in mice and humans.