Sensing and Reacting to Microbes via the Inflammasomes

By L. Franchi, Raúl Muñoz-Planillo, G. Núñez. Nature Immunology, 2012

986 citations recorded by the source corpus.

Inflammasomes are multiprotein complexes that activate caspase-1, which leads to maturation of the proinflammatory cytokines interleukin 1β (IL-1β) and IL-18 and the induction of pyroptosis. Members of the Nod-like receptor (NLR) family, including NLRP1, NLRP3 and NLRC4, and the cytosolic receptor AIM2 are critical components of inflammasomes and link microbial and endogenous danger signals to the activation of caspase-1. In response to microbial infection, activation of the inflammasomes contributes to host protection by inducing immune responses that limit microbial invasion, but deregulated activation of inflammasomes is associated with autoinflammatory syndromes and other pathologies. Thus, understanding inflammasome pathways may provide insight into the mechanisms of host defense against microbes and the development of inflammatory disorders.

Subfields: Molecular Biology, Public Health, Environmental and Occupational Health

View Paper: https://www.semanticscholar.org/paper/0a063c902fe000973d50fddd037709938ff7f2c8

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Citations in the corpus

Initiation and perpetuation of NLRP3 inflammasome activation and assembly (2015, background): “Additionally, the NLRP3 inflammasome recognizes and responds to infection with numerous bacteria, viruses, fungi, and parasites (16).”
Regulated cell death (RCD) in cancer: key pathways and targeted therapies (2022, background): “The activation of the classical pyroptosis pathway is initiated by pathogen-associated molecular patterns (PAMPs) or sterile molecular patterns (DAMPs).(37,38) They are recognized by cytoplasmic pattern recognition receptors (PRRS).”
Mechanism and regulation of NLRP3 inflammasome activation (2016, background): “During microbial infections, the NLRP3 inflammasome promotes host immune defense against infectious microbes such as influenza A virus, Staphylococcus aureus, andCandida albicans [1].”
Cell Death Signaling. (2015, background): “crystals, calcium phosphate crystals, alum, asbestos) (Franchi et al. 2012).”
Neutrophil cell surface receptors and their intracellular signal transduction pathways (2013, neutral): “5) [221,222].”
Non-transcriptional Priming and Deubiquitination Regulate NLRP3 Inflammasome Activation* (2012, background): “Inflammasomes are key components of the innate immune response to tissue damage or infection by microbial or viral pathogens (1).”
NLRP3 inflammasome and its inhibitors: a review (2015, background): “…PAMPs or DAMPs are recognized by TLRs, leading to activation of nuclear factor kappa B (NF-κB)-mediated signaling, which in turn up-regulates transcription of inflammasome-related components, including inactive NLRP3, proIL-1β, and proIL18 (Bauernfeind et al., 2009; Franchi et al., 2012, 2014).”
Unified Polymerization Mechanism for the Assembly of ASC-dependent Inflammasomes (2014, background): “The best-studied NLRP3 inflammasome is activated following a wide range of pathogen and danger signals, including extracellular ATP and uric acid crystals (Franchi et al., 2012; Lamkanfi and Dixit, 2012; Rathinam et al., 2012).”
TRIF Licenses Caspase-11-Dependent NLRP3 Inflammasome Activation by Gram-Negative Bacteria (2012, positive): “The cytosolic compartment in particular has emerged as a frontline of host defense, where distinct families of receptors recognize microbial products and initiate protective immune defenses (Franchi et al., 2012; Rathinam and Fitzgerald, 2011).”