Mechanism of NLRP3 inflammasome activation
Open accessAbstract
Inflammasomes continue to generate interest in an increasing number of disciplines owing to their unique ability to integrate a myriad of signals from pathogen- and damage-associated molecular patterns into a proinflammatory response. This potent caspase-1-dependent process is capable of activating the innate immune system, initiating pyroptosis (an inflammatory form of programmed cell death), and shaping adaptive immunity. The NLRP3 inflammasome is the most thoroughly studied of the inflammasome complexes that have been described thus far, perhaps owing to its disparate assortment of agonists. This review highlights our current understanding of the mechanisms of both priming and activation of the NLRP3 inflammasome.
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This binding elicits activation of the NLRP3 inflammasome in LPS-stimulated macrophages, causing secretion of IL-18 and IL-1β, and may promote maintenance and function of the epithelial barrier.
“this has been shown to elicit activation of the NLRP3 inflammasome in LPS-stimulated macrophages, which causes secretion of IL-18 (but also of the pro-inflammatory cytokine IL-1β) and may thus promote maintenance and function of the epithelial barrier (Mariathasan et al., 2006; Sutterwala et al., 2014; 2006; Yaron et al., 2015).”
From Understanding the Holobiont: How Microbial Metabolites Affect Human Health and Shape the Immune System (2017) · cites this paper as Sutterwala et al., 2014
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“Activation of the NLRP3 inflammasome appears to occur in two steps (Zhong et al., 2013a; Sutterwala et al., 2014; Ozaki et al., 2015; Figure 1).”
BackgroundInitiation and perpetuation of <scp>NLRP</scp> 3 inflammasome activation and assembly
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Self-citationThe NLRP3 inflammasome in acute myocardial infarction
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Pharmacological Inhibitors of the NLRP3 Inflammasome
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Inflammasome activation leads to Caspase-1–dependent mitochondrial damage and block of mitophagy
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Inflammasome, pyroptosis, and cytokines in myocardial ischemia-reperfusion injury
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“NLRs, including the NLRP1, NLRP3 and NLR family caspase recruitment domain (CARD) domain containing 4 (NLRC4) inflammasomes, are characterized by a central located NOD domain that is flanked at N-terminal CARD, pyrin domain (PYD), acidic transactivating domain, or baculovirus inhibitor repeat (BIR) (Franchi et al., 20…”
BackgroundExosome-like Nanoparticles from Ginger Rhizomes Inhibited NLRP3 Inflammasome Activation
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Spotlight on the NLRP3 inflammasome pathway
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Multiple cathepsins promote pro-IL-1β synthesis and NLRP3-mediated IL-1β activation
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K+ regulates Ca2+ to drive inflammasome signaling: dynamic visualization of ion flux in live cells
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“Proposed mechanisms for regulating the activation of the NLRP3 inflammasome pathway are varied and controversial.(1) Among the most popular proposed mechanisms is the flux of cellular ions.”
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Ginsenoside Rg1 attenuates cardiomyocyte apoptosis and inflammation via the TLR4/NF‐kB/NLRP3 pathway
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The NLRP3 inflammasome is critically involved in the development of bronchopulmonary dysplasia
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Fasting and refeeding differentially regulate NLRP3 inflammasome activation in human subjects
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Recent Advances of the NLRP3 Inflammasome in Central Nervous System Disorders
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Pyroptosis is a critical immune-inflammatory response involved in atherosclerosis.
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- Authors
- Sutterwala, F. S., Haasken, S., & Cassel, S. L.
- Affiliations
- University of Iowa (US)
- Corresponding author
- Sutterwala, Fayyaz S.
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2014-05-19
- Volume
- 1319
- Issue
- 1
- Pages
- 82-95
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC4074217
- OpenAlex
- W1636793459
- Cited by
- 736
- References
- 82
- Citations by year
- 2026: 25 · 2025: 54 · 2024: 58 · 2023: 68 · 2022: 85 · 2021: 88 · 2020: 81 · 2019: 52 · 2018: 60 · 2017: 57 · 2016: 57 · 2015: 42 · 2014: 8
- FWCI
- 5.18
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AI087630, AI104706, AI007511)
- Asthma and Allergy foundation of America
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- NLRP3 inflammasome, inflammasome activation, inflammasome priming, caspase-1, pyroptosis, innate immunity, damage-associated molecular patterns, pathogen-associated molecular patterns
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Carrier Proteins, Cell Survival, Humans, Cell Death, Adaptive Immunity, Inflammasomes
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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