Necrotic cells trigger a sterile inflammatory response through the Nlrp3 inflammasome

By S. Iyer, W. Pulskens, J. Sadler, L. Butter, G. Teske, Tyler K. Ulland, S. Eisenbarth, S. Florquin, R. Flavell, J. Leemans and 1 more. Proceedings of the National Academy of Sciences of the United States of America, 2009

720 citations recorded by the source corpus.

Subfields: Molecular Biology, Pediatrics, Perinatology and Child Health

View Paper: https://www.semanticscholar.org/paper/e9af6327400a2736b61b9630c04c503b85436e41

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In Molecular Biology

In Pediatrics, Perinatology and Child Health

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Citations in the corpus

Mitochondria in innate immune responses (2011, background): “A recent study demonstrates a role for mitochondria in NLRP3 inflammasome activatio”
The role of oxidative stress during inflammatory processes (2013, background): “…is also activated during tissue injury, mainly by hyaluronan released from damaged ECM (Yamasaki et al., 2009) and by ATP released by dying cells (Iyer et al., 2009; Silverman et al., 2009; Riteau et al., 2010; Davis et al., 2011), fostering the development of sterile inflammation in…”
Immunogenic cell death and DAMPs in cancer therapy (2012, background): “These authors showed that a recombinant N-terminal fragment of CRT (39-272) is a potent inducer of activation and maturation of B cells and macrophages and can trigger Ig class switching in B cells without T cell help in vitro and in vivo72.”
Mitochondrial cardiolipin is required for Nlrp3 inflammasome activation (2013, methodology): “Recent studies have demonstrated that necrotic cells are capable of inducing macrophage inflammasome activation (Ghiringhelli et al., 2009; Iyer et al., 2009).”
The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse (2011, background): “Release of active IL-1β from activated leukocytes or endothelial cells following formation of the inflammasome triggers a sterile inflammation response that amplifies the initial injury (25, 26).”
The Inflammasome NLRs in Immunity, Inflammation, and Associated Diseases (2011, background): “Extracellular ATP, uric acid, P2X7 receptor, and IL-1β are involved in chronic and atopic lung inflammation (37--41), whereas ATP, P2X7 receptor, mitochondria, and hyaluron are associated with ischemia-reperfusion injury activation of the NLRP3 inflammasome (27).”
Vaccine Adjuvants: Putting Innate Immunity to Work (2010, background): “Necrotic cells release ATP and uric acid, which activate the NLRP3 inflammasome, thereby linking cellular damage to an inflammatory response (Hornung et al., 2008; Iyer et al., 2009).”
Ischemia and reperfusion—from mechanism to translation (2011, background): “Many of these ligands (for example, high-mobility group box 1 (HMGB1) protein or ATP) are normally sequestered intracellularly; upon tissue damage, they are released into the extracellular compartment where they can activate an immune respons”
Sterile inflammation: sensing and reacting to damage (2010, background): “NLRP3-deficient mice were also less susceptible to renal ischaemia–reperfusion injuries induced by bilateral renal artery ligation and to acetaminophen-induced hepatotoxicit”
Immunity, atherosclerosis and cardiovascular disease (2013, background): “Dying cells can activate the innate immune system and induce an inflammatory response with release of the proinflammatory cytokine IL-1beta, activating the inflammasome [30].”