Nlrp3: An immune sensor of cellular stress and infection
Open accessAbstract
Innate immune cells rely on pathogen recognition receptors such as the nucleotide-binding and oligomerization domain (NOD)-like receptor (NLR) family to mount an appropriate immune response against microbial threats. The NLR protein Nlrp3 senses microbial ligands, endogenous danger signals and crystalline substances in the cytosol to trigger the assembly of a large caspase-1-activating protein complex termed the Nlrp3 inflammasome. Autoproteolytic maturation of caspase-1 zymogens in the Nlrp3 inflammasome leads to maturation and extracellular release of the pro-inflammatory cytokines interleukin (IL)-1beta and IL-18. Gain-of-function mutations in the NOD domain of Nlrp3 are associated with auto-inflammatory disorders characterized by skin rashes and prolonged episodes of fever. In addition, decreased Nlrp3 expression was recently linked with susceptibility to Crohn's disease in humans. In this review, we discuss recent developments on the role of the Nlrp3 inflammasome in innate immunity, its activation mechanisms and the auto-inflammatory disorders associated with deregulation of Nlrp3 inflammasome activity.
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Because wide-ranging stimuli for NLRP3 are structurally and chemically dissimilar, it is unlikely that NLRP3 binds to these stimuli directly.
“Because the wide-ranging stimuli for NLRP3 (e.g., ATP, toxins, RNA virus, K+ ionophores) are structurally and chemically dissimilar,351 it is unlikely that NLRP3 binds to these stimuli directly.”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [351]
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- Authors
- Lamkanfi, M., & Kanneganti, T.-D.
- Affiliations
- Ghent University (BE)
- St. Jude Children's Research Hospital (US)
- Corresponding author
- Kanneganti, Thirumala-Devi
- Venue
- The International Journal of Biochemistry & Cell Biology
- Publisher
- Elsevier BV
- Published
- 2010-06
- Volume
- 42
- Issue
- 6
- Pages
- 792-795
- ISSN
- 1357-2725 (ISSN-L)
- PMC
- PMC2862759
- OpenAlex
- W2160038863
- Cited by
- 140
- References
- 32
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 7 · 2023: 8 · 2022: 13 · 2021: 16 · 2020: 6 · 2019: 9 · 2018: 8 · 2017: 12 · 2016: 5 · 2015: 7 · 2014: 4 · 2013: 11 · 2012: 4
- FWCI
- 0.90
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- The International Journal of Biochemistry & Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Ghent University Academic Bibliography (Ghent University) (submittedVersion)
- Funders
- American Lebanese Syrian Associated Charities
- 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 › interferon and immune responses
- Keywords
- NLRP3, NLRP3 inflammasome, NOD-like receptors, innate immunity, caspase-1, IL-1β, IL-18, Crohn's disease, pathogen recognition, damage-associated molecular patterns, inflammasome activation
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Autoimmune Diseases, Carrier Proteins, Disease Susceptibility, Humans, Immunity, Innate, Infections, Inflammation, Polymorphism, Genetic, Stress, Physiological, Multiprotein Complexes, Host-Pathogen Interactions
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