The NLRP3 inflammasome is released as a particulate danger signal that amplifies the inflammatory response
By A. Baroja-Mazo, Fátima Martín-Sánchez, A. I. Gómez, C. Martínez, Joaquín Amores-Iniesta, V. Compan, M. Barberà-Cremades, J. Yagüe, E. Ruiz-Ortiz, J. Antón and 5 more. Nature Immunology, 2014
777 citations recorded by the source corpus.
Subfields: Hematology, Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/49d1e126c97f60896e19265c762204a3eeb3ff75
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Hematology
In Immunology
In Molecular Biology
Citations in the corpus
- The Phagocytic Function of Macrophage-Enforcing Innate Immunity and Tissue Homeostasis (2017, background): “It was revealed that extensive complexation aggravated inflammation by activating the production of inflammatory cytokines [7,8].”
- Regulation of inflammasome activation (2015, background): “In addition, they are phagocytosed by neighboring macrophages and serve as an endogenous danger signal to trigger a second wave of inflammasome activation (194, 195).”
- Inflammasomes in neuroinflammatory and neurodegenerative diseases (2019, background): “In addition, NLRP3 inflammasome activity also results in the extracellular release of micrometer-sized ASC particles that may function as danger signals and alert surrounding macrophages (Baroja-Mazo et al, 2014).”
- Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “The dynamics of release differ among components with monomeric ASC and caspase-1 resembling IL-1b release, and NLRP3 and ASC speck release correlating with LDH release and requiring caspase-1-dependent cell death (162, 177).”