Cited by 281Inflammasome and immune disordersImmune Response and InflammationIL-33, ST2, and ILC Pathways

Sensing damage by the NLRP3 inflammasome

Open access
Leemans, Jaklien C., Cassel, Suzanne L., Sutterwala, Fayyaz S.·2011·Immunological Reviews

Abstract

Summary: The NLRP3 inflammasome is activated in response to a variety of signals that are indicative of damage to the host including tissue damage, metabolic stress, and infection. Upon activation, the NLRP3 inflammasome serves as a platform for activation of the cysteine protease caspase‐1, which leads to the processing and secretion of the proinflammatory cytokines interleukin‐1β (IL‐1β) and IL‐18. Dysregulated NLRP3 inflammasome activation is associated with both heritable and acquired inflammatory diseases. Here, we review new insights into the mechanism of NLRP3 inflammasome activation and its role in disease pathogenesis.

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Crossref · 10.1111/j.1600-065x.2011.01043.x

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  • The NLRP3 inflammasome is implicated in a diverse array of sterile inflammatory diseases including ischemia-reperfusion injury, autoinflammatory diseases, type 2 diabetes, gout and pseudogout, obesity, atherosclerosis, and Alzheimer's disease.

    “The NLRP3 inflammasome has been implicated in a diverse array of sterile inflammatory diseases including ischemia-reperfusion injury, autoinflammatory diseases, type 2 diabetes, gout and pseudogout, obesity, atherosclerosis, and Alzheimer's disease (Leemans et al, 2011)”
  • Sterile inflammation is driven in large part by DAMPs that are released after physical and psychological stressors.

    “sterile inflammation is driven in large part by DAMPs that are released after physical and psychological stressors (Leemans et al, 2011).”
  • The LRR domain on the NLR is sensitive to a diverse array of danger signals, including ATP.

    “The LRR domain is sensitive to a diverse array of danger signals, including ATP (Leemans et al, 2011).”

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  1. [41]Kaczorowski DJ Tsung A Billiar TR Innate immune mechanisms in ischemia/reperfusion Front Biosci 2009 1 91 98 19482628

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Authors
Leemans, J. C., Cassel, S. L., & Sutterwala, F. S.
Affiliations
  • Amsterdam UMC Location University of Amsterdam (NL)
  • University of Iowa (US)
Corresponding author
Sutterwala, Fayyaz S.
Venue
Immunological Reviews
Publisher
Wiley
Published
2011-08-26
Volume
243
Issue
1
Pages
152-162
ISSN
  • 0105-2896 (ISSN-L)
  • 1600-065X
OpenAlex
W2171212614
Cited by
281
References
99
Citations by year
2026: 7 · 2025: 14 · 2024: 5 · 2023: 14 · 2022: 15 · 2021: 13 · 2020: 14 · 2019: 27 · 2018: 26 · 2017: 17 · 2016: 30 · 2015: 34 · 2014: 22 · 2013: 24 · 2012: 16
FWCI
1.86
Type
journal article
Language
en
Open access
Locations
  • Immunological Reviews (publishedVersion)
  • PubMed (publishedVersion)
  • Pure Amsterdam UMC (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Data Archiving and Networked Services (DANS) (submittedVersion)
Funders
National Institute of Allergy and Infectious Diseases (R01AI087630, K08AI067736)
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, caspase-1, IL-1β, IL-18, metabolic stress, infection, inflammatory diseases, pathogenesis
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Autoimmune Diseases, Carrier Proteins, Humans, Immunity, Innate, Infections, Inflammation, Stress, Physiological, Caspases, Interleukin-18, Interleukin-1beta, Inflammasomes

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