Cited by 142Inflammasome and immune disordersImmune Response and Inflammationinterferon and immune responses

Nlrp3: An immune sensor of cellular stress and infection

Open access
Lamkanfi, Mohamed, Kanneganti, Thirumala-Devi·2010·The International Journal of Biochemistry & Cell Biology

Abstract

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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Crossref · 10.1016/j.biocel.2010.01.008

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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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  1. Kawai T Akira S TLR signaling Cell Death Differ 2006 13 816 825 16410796

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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)
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
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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