Inflammasome adaptors and sensors: intracellular regulators of infection and inflammation

By S. Mariathasan, D. Monack. Nature reviews. Immunology, 2007

921 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/9ede19218de5dbc3825cac301a1b7668a5b077c7

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Citations in the corpus

The inflammatory response to cell death. (2008, background): “Therefore, IL-1 is a particularly important host mediator in the acute neutrophilic inflammatory response to dead cells.”
The NALP3 inflammasome is involved in the innate immune response to amyloid-β (2008, methodology): “As controls, we used cells from wild-type mice and mice deficient in Ipaf, which is part of a different inflammasome typically activated by intracellular bacterial pathogen”
The NLRP3 Inflammasome Mediates in vivo Innate Immunity to Influenza A Virus through Recognition of Viral RNA (2009, background): “In addition to NLRP3, other NLRs such as NLRC4 and NLRP1 also cause caspase-1 activation and IL-1β production (Mariathasan and Monack, 2007).”
Pyroptosis: host cell death and inflammation (2009, neutral): “Aluminium-containing adjuvants also stimulate caspase 1 activatio”
Pattern-recognition receptors in plant innate immunity. (2008, background): “It is also unknown whether some of the 150 cytoplasmic NBSLRR proteins present in Arabidopsis [55], for example, could also act as intracellular PRRs, as recently demonstrated in mammals [56].”
The pyroptosome: a supramolecular assembly of ASC dimers mediating inflammatory cell death via caspase-1 activation (2007, background): “Caspase-1 is activated by cytosolic complexes termed inflammasomes.(5,6) In the past few years a number of inflammasome complexes have been identified including ICE-protease activating factor (IPAF), NALP1, NALP2, cryopyrin/NALP3, and pyrin inflammasomes.”
Dectin-1 is an extracellular pathogen sensor for the induction and processing of IL-1β via a noncanonical caspase-8 inflammasome (2012, background): “As a control, caspase-1 inhibition completely impaired the processing of pro-IL-1β after treatment of DCs with lipopolysaccharide (LPS) and ATP, a known activator of the NLRP3 inflammasome, or flagellin, which activates the NLRC4 inflammasom”
IL‐1, IL‐18, and IL‐33 families of cytokines (2008, background): “The first signal appears to be TLR induction of transcription of pro-IL-1b with subsequent storage in the cell (6, 7).”
Macrophage activation by endogenous danger signals (2008, background): “In the past few years, much attention has centred on deciphering the signalling pathways initiated by NOD1 and NOD2 [33].”
The endogenous Toll–like receptor 4 agonist S100A8/S100A9 (calprotectin) as innate amplifier of infection, autoimmunity, and cancer (2009, background): “Like PAMPs, DAMPs are recognized by PRRs. Interestingly, some receptors such as the TLR4 seem to be able to recognize PAMPs as well as DAMPs [8, 9].”
The Nalp3 inflammasome is essential for the development of silicosis (2008, background): “The mammalian NLR family is composed of over 20 members that contain a C-terminal leucine-rich repeat (LRR) domain, a central nucleotide-binding NACHT domain, and an N-terminal protein–protein-interaction domain composed of a CARD (caspase activation and recruitment domain) or pyrin domain (9, 10).”
Molecular Pathogenesis of Shigella spp.: Controlling Host Cell Signaling, Invasion, and Death by Type III Secretion (2008, background): “Extensive research over the last years described the inflammasome as being a dynamic multiprotein complex (160, 162).”