The Inflammasome: A Caspase-1 Activation Platform Regulating Immune Responses and Disease Pathogenesis
By L. Franchi, T. Eigenbrod, Raúl Muñoz-Planillo, G. Núñez. Nature Immunology, 2009
1,836 citations recorded by the source corpus.
The inflammasome is a multiprotein complex that mediates the activation of caspase-1, which promotes secretion of the proinflammatory cytokines interleukin 1β (IL-1β) and IL-18, as well as 'pyroptosis', a form of cell death induced by bacterial pathogens. Members of the Nod-like receptor family, including NLRP1, NLRP3 and NLRC4, and the adaptor ASC are critical components of the inflammasome that link microbial and endogenous 'danger' signals to caspase-1 activation. Several diseases are associated with dysregulated activation of caspase-1 and secretion of IL-1β. Thus, understanding inflammasome pathways may provide insight into disease pathogenesis that might identify potential targets for therapeutic intervention.
Subfields: Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/be1504d5125b6614fcdd9f8bec093df0aada0eba
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In Molecular Biology
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In Surgery
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Citations in the corpus
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- Pathogen Recognition by the Innate Immune System (2011, background): “Recently, several reports showed that the pathogenic fungus, Candida, and baker’s yeast (Saccharomyces) induced IL-1β via NLRP3, ASC and caspase-1, and further studies revealed that β-glucan, a major component of fungal cell walls, activates the NLRP3 inflammasome [108–115].”
- Critical role for calcium mobilization in activation of the NLRP3 inflammasome (2012, neutral): “Stauffer TP, Ahn S, Meyer T (1998) Receptor-induced transient reduction in plasma membrane PtdIns(4,5)P2 concentration monitored in living cells.”
- The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse (2011, background): “Cryopyrin activation leads to recruitment of the apoptosis speck-like protein containing a caspase-recruitment domain (ASC) and formation of the inflammasome, a multiprotein complex necessary for caspase-1 activation and interleukin-1β (IL-1β) release (7, 8).”
- Neutrophil cell surface receptors and their intracellular signal transduction pathways (2013, neutral): “5) [221,222].”
- The NLRP3 Inflammasome: An Overview of Mechanisms of Activation and Regulation (2019, background): “The activation of inflammasomes, a group of intracellular multimeric protein complexes that activate inflammatory caspase-1, is a major inflammatory pathway [2].”
- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Thus, pyroptosis is often (if not always) associated with IL-1β and IL18 secretion, and hence mediates robust pro-inflammatory effects [614, 615].”
- Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012 (2011, background): “context of a multiprotein platform known as the inflammasome, which involves the adaptor protein ASC and NOD-like receptors (NLRs) or the cytosolic DNA sensor absent in melanoma 2 (AIM2).(147,151,152) Alternatively, caspase-1 can be activated by the so-called pyroptosome, a supramolecular assembly o”