Pyroptotic cell death defends against intracellular pathogens

By Ine Jorgensen, Edward A. Miao. Immunological Reviews, 2015

929 citations recorded by the source corpus.

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.

Subfields: Immunology, Molecular Biology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/68b6cef2c0e2ee27124eab3d61fce784820a1080

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Citations in the corpus

ZBP1/DAI is an innate sensor of influenza virus triggering the NLRP3 inflammasome and programmed cell death pathways (2016, positive): “In addition, virus sensing also induces cell death in order to destroy the replicative niche necessary for survival and propagation of these intracellular pathogens (3).”
Pattern Recognition Receptors and the Host Cell Death Molecular Machinery (2018, background): “against pathogens, the precise contribution of pyroptosis and other inflammasome-related mechanisms are poorly understood and arose mainly from in vitro assays or bacterial infection models in mice deficient for molecules that compose these platforms (159, 175).”
Mechanisms and disease consequences of nonalcoholic fatty liver disease (2021, background): “Pyroptosis is a specialized form of cell death in NASH that is similar to the action of inflammatory caspases and, like necroptosis, induces cell swelling and release of inflammatory signals (Beier and Banales, 2018; Jorgensen and Miao, 2015).”
Pyroptosis: Gasdermin-Mediated Programmed Necrotic Cell Death. (2017, background): “membrane [6], but the necrotic nature only became generally accepted in recent years.”
Structural Mechanism for GSDMD Targeting by Autoprocessed Caspases in Pyroptosis. (2020, background): “Pyroptosis is a lytic cell death induced by pathogen infection or endogenous challenge (Broz and Dixit, 2016; Jorgensen and Miao, 2015; Rathinam et al., 2019).”
NLRP3 inflammasome and its inhibitors: a review (2015, background): “A newly identified PRR, first described in detail in 2002, is the inflammasome (Martinon et al., 2002; Gentile et al., 2015; Jorgensen and Miao, 2015; Sanders et al., 2015).”
Gasdermins: Effectors of pyroptosis (2017, background): “For example, the NAIP/NLRC4 inflammasome detects bacterial type III and type IV secretion systems when they aberrantly inject rod, needle, or flagellin protein into the cytosol[74].”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “ever, recent findings indicate that pyroptosis (1) can be also driven by several other caspases including CASP3 [608], (2) can also occur in cell types other than cells from the monocytic lineage [609], (3) has a major role in innate immunity against intracellular pathogens [602], and (4) is etiolog”