The inflammasome: an integrated view

By O. Gross, Christina J. Thomas, Greta Guarda, J. Tschopp. Immunological Reviews, 2011

770 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/dc5e19925e2a512045461f8532ea9995c621e00d

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Citations in the corpus

Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke. (2016, background): “…(Mohamed et al., 2015; Schroder and Tschopp, 2010), which in turn further cleaves immature proinflammatory cytokines IL-1β and IL-18 into mature cytokines for release into the extracellular environment where they are involved in inflammatory responses (Gross et al., 2011; Tsuchiya and Hara, 2014).”
The adapter MAVS promotes NLRP3 mitochondrial localization and inflammasome activation (2013, neutral): “NLRP3 forms a macromolecular signaling complex called the inflammasome upon activation by a variety of signals, including infection and metabolic dysregulation, but how these chemically and structurally diverse entities elicit a response from a single sensor molecule is unclear (Gross et al., 2011).”
NLRP3 inflammasome: From a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases (2015, background): “…Univ Paris 06, UMR 8256, Biological Adaptation and Ageing - IBPS, F-75005 Paris, France b CNRS-UMR 8256, F-75005 Paris, France c Inserm U1164, F-75005 Paris, France d Institute of Pharmacology of Natural Products & Clinical Pharmacology, Ulm University, D-89081 Ulm, Germany a r t i c l e i n f o”
Staphylococcus aureus Leukocidin A/B (LukAB) Kills Human Monocytes via Host NLRP3 and ASC when Extracellular, but Not Intracellular (2015, background): “Only recently has the role of inflammasomes in other phagocytic and non-immune cells begun to be evaluated [49,50].”
Omega-3 fatty acids prevent inflammation and metabolic disorder through inhibition of NLRP3 inflammasome activation. (2013, background): “K efflux, elevated ROS levels, mitochondria damage, and lysosomal rupture have been proposed to participate in NLRP3 inflammasome activation (Gross et al., 2011; Zhou et al., 2011), but we still know very little about the precise mechanisms that can positively or negatively regulate NLRP3 inflammaso”
Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosis. (2012, background): “The second signal, any one of a variety of unrelated entities—particulate matter, crystals, aggregated b-amyloid, extracellular ATP, or microbial toxins—activates the NLRP3 inflammasome (Gross et al., 2011).”