Mechanism and regulation of NLRP3 inflammasome activation

By Yuan He, H. Hara, G. Núñez. TIBS -Trends in Biochemical Sciences. Regular ed, 2016

2,450 citations recorded by the source corpus.

Members of the nucleotide-binding domain and leucine-rich repeat containing (NLR) family and the pyrin and HIN-domain (PYHIN) family can form multiprotein complexes termed “inflammasomes”. The biochemical function of inflammasomes is to activate caspase-1, which leads to the maturation of interleukin 1β (IL-1β) and IL-18 and induction of pyroptosis, a form of cell death. Unlike other inflammasomes, the NLRP3 inflammasome can be activated by diverse stimuli. The importance of the NLRP3 inflammasome in immunity and human diseases has been well documented, but the mechanism and regulation of NLRP3 inflammasome activation remains unclear. In this review we summarize current understanding of the mechanism and regulation of NLRP3 inflammasome activation, as well as recent advances in the non-canonical and alternative inflammasome pathways.

Subfields: Immunology, Molecular Biology, Nephrology

View Paper: https://www.semanticscholar.org/paper/b6c138c5c94e4f5bcb3fe53b0c4ca6fb897f2e2e

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In Immunology

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Citations in the corpus

Pattern recognition receptors in health and diseases (2021, background): “NLR agonists can promote the processing and secretion of IL-1β, which is very important for activating many immune cells.(449,450) Therefore, NLR agonists can be served as effective components of vaccines and immune stimulants.”
NF-κB signaling in inflammation (2017, positive): “61 NF-κ B is a central mediator of the priming signal of NLRP3 inflammasome activation and acts by inducing the transcriptional expression of NLRP3 and pro-IL-1 β in response to various PRR ligands and cytokines.”