Bacterial RNA and small antiviral compounds activate caspase-1 through cryopyrin/Nalp3

By T. Kanneganti, Nesrin Özören, Mathilde Body-Malapel, A. Amer, Jong-Hwan Park, L. Franchi, J. Whitfield, W. Barchet, M. Colonna, Peter Vandenabeele and 5 more. Nature, 2006

1,230 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Nephrology

View Paper: https://www.semanticscholar.org/paper/6b92e696185d99545891a5f198ae3e0ee9fbc847

How researchers see this paper

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In Immunology

1. J. Tschopp
2. T. Kanneganti
3. M. Lamkanfi
4. G. Núñez
5. Guido Kroemer
6. L. Zitvogel
7. E. Latz
8. V. Dixit

In Molecular Biology

1. J. Tschopp
2. T. Kanneganti
3. G. Núñez
4. M. Lamkanfi
5. C. A. Dinarello
6. V. Dixit
7. E. Latz
8. Kate Schroder

In Nephrology

1. J. Tschopp
2. G. Núñez
3. H. Kono
4. K. Rock
5. T. Kanneganti
6. E. Latz
7. Guido Kroemer
8. Kate Schroder

Citations in the corpus

• Activation of the NLRP3 inflammasome in dendritic cells induces IL-1β–dependent adaptive immunity against tumors (2009, background): “Multiple distinct bacterial products or endogenous damage signals stimulate the NLRP3 inflammasome, resulting in the proteolytic activation of caspase-”
• Nonclassical IL-1β Secretion Stimulated by P2X7 Receptors Is Dependent on Inflammasome Activation and Correlated with Exosome Release in Murine Macrophages1 (2007, background): “DNA, flagellin (12–14), bacterial RNA (15), viral RNA (16), and”
• Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration (2007, background): “For example, bacterial muramyl dipeptide (MDP),(15) a degradation product of the bacterial cell wall component peptidoglycans (PGN), as well as RNA of bacterial and viral origin activate NALP3.(16,17) Besides these classical PAMPs, the microbial toxins nigericin (Streptomyces hygroscopicus), aerolys”
• Glyburide inhibits the Cryopyrin/Nalp3 inflammasome (2009, background): “…macrophage; DAMP, danger-associated molecular pattern; FCAS, familial cold-associated autoinflammatory syndrome; IL, interleukin; KATP, ATP-sensitive K+; LPS, lipopolysaccharide; PAMP, pathogen-associated molecular pattern; PBMC, peripheral blood mononuclear cell; SUR, sulfonylurea receptor.”
• The pyroptosome: a supramolecular assembly of ASC dimers mediating inflammatory cell death via caspase-1 activation (2007, methodology): “LPS and bacterial Pam3CSK4 or FSL-1 lipopeptides have been shown recently to induce caspase-1 activation and IL-1b secretion from mouse bone marrow macrophages independent of the cryopyrin inflammasome.(13) To investigate if signals that activate the cryopyrin inflammasome could also induce the form”
• Silica crystals and aluminum salts mediate NALP-3 inflammasome activation via phagosomal destabilization (2008, methodology): “We pretreated human PBMCs with cytochalasin D, a well characterized inhibitor of phagocytosis that impairs actin filament assembly, and then stimulated the cells with MSU or silica crystals as well as with two noncrystalline NALP3 activators, the imidazoquinoline derivative R-848 and AT”
• Pathogen recognition and innate immunity. (2006, neutral): “The ligands for NALP family members are currently unknown, except for NALP3, which is involved in the recognition of bacterial RNA, ATP, and uric-acid crystals (Kanneganti et al., 2006; Mariathasan et al., 2006; Martinon et al., 2006).”