Cited by 458Inflammasome and immune disordersImmune Response and InflammationCell death mechanisms and regulation

A 360° view of the inflammasome: Mechanisms of activation, cell death, and diseases

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Barnett, Katherine C., Li, Sirui, Liang, Kaixin, Ting, Jenny P.-Y.·2023·Cell

Abstract

Inflammasomes are critical sentinels of the innate immune system that respond to threats to the host through recognition of distinct molecules, known as pathogen- or damage-associated molecular patterns (PAMPs/DAMPs), or disruptions of cellular homeostasis, referred to as homeostasis-altering molecular processes (HAMPs) or effector-triggered immunity (ETI). Several distinct proteins nucleate inflammasomes, including NLRP1, CARD8, NLRP3, NLRP6, NLRC4/NAIP, AIM2, pyrin, and caspases-4/-5/-11. This diverse array of sensors strengthens the inflammasome response through redundancy and plasticity. Here, we present an overview of these pathways, outlining the mechanisms of inflammasome formation, subcellular regulation, and pyroptosis, and discuss the wide-reaching effects of inflammasomes in human disease.

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  • NLRP3 inflammasome activation initiates assembly and caspase-1 activation, leading to GSDMD-mediated pore formation, release of IL-1β and IL-18, and pyroptotic cell death.

    “This initiates inflammasome assembly and caspase-1 activation, leading to gasdermin-D (GSDMD)-mediated pore formation, the release of interleukin (IL)-1β and IL-18, and pyroptotic cell death.27”

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Cited by

Sorted by citations

Authors
Barnett, K. C., Li, S., Liang, K., & Ting, J. P.-Y.
Affiliations
University of North Carolina at Chapel Hill (US)
Corresponding author
  • Barnett, Katherine C.
  • Ting, Jenny P.-Y.
Venue
Cell
Publisher
Elsevier BV
Published
2023-05
Volume
186
Issue
11
Pages
2288-2312
ISSN
0092-8674 (ISSN-L)
OpenAlex
W4378212976
Cited by
458
References
30
Citations by year
2026: 131 · 2025: 161 · 2024: 136 · 2023: 29 · 2022: 1
FWCI
12.07
Type
journal article
Language
en
Open access
Locations
  • Cell (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health (DK094779, AI029564, AI067798)
  • National Cancer Institute (R35CA232109)
  • National Institute of Allergy and Infectious Diseases (R01AI141333, R37AI029564, U19AI067798, R56AI158314, R56AI029564, R01AI029564, R01AI158314)
  • National Institute of Diabetes and Digestive and Kidney Diseases (P01DK094779)
  • National Institute of Environmental Health Sciences (R01ES032643)
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 › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Keywords
inflammasome, inflammasome activation, pyroptosis, NLRP3 inflammasome, NLRP1, CARD8, NLRP6, NLRC4, NAIP, AIM2, pyrin, caspase-1, caspase-5, caspase-11, innate immunity, pathogen-associated molecular patterns, damage-associated molecular patterns, effector-triggered immunity
MeSH terms
Pyroptosis, NLR Family, Pyrin Domain-Containing 3 Protein, Humans, Neoplasm Proteins, Cell Death, Caspases, Apoptosis Regulatory Proteins, CARD Signaling Adaptor Proteins, Inflammasomes

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