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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 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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Metadata
- 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
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- 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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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