Cited by 1,378Inflammasome and immune disordersImmune Response and InflammationIL-33, ST2, and ILC Pathways

Molecular mechanisms regulating NLRP3 inflammasome activation

Open access
Jo, Eun-Kyeong, Kim, Jin Kyung, Shin, Dong-Min, Sasakawa, Chihiro·2016·Cellular & Molecular Immunology

Abstract

Inflammasomes are multi-protein signaling complexes that trigger the activation of inflammatory caspases and the maturation of interleukin-1β. Among various inflammasome complexes, the NLRP3 inflammasome is best characterized and has been linked with various human autoinflammatory and autoimmune diseases. Thus, the NLRP3 inflammasome may be a promising target for anti-inflammatory therapies. In this review, we summarize the current understanding of the mechanisms by which the NLRP3 inflammasome is activated in the cytosol. We also describe the binding partners of NLRP3 inflammasome complexes activating or inhibiting the inflammasome assembly. Our knowledge of the mechanisms regulating NLRP3 inflammasome signaling and how these influence inflammatory responses offers further insight into potential therapeutic strategies to treat inflammatory diseases associated with dysregulation of the NLRP3 inflammasome.

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Registry

Crossref · 10.1038/cmi.2015.95

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139 of 139 references verified0 citation errors · 0 not checkable

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  • ATP may act as a DAMP, which activates the nuclear transcription factor NF-κB, resulting in expression upregulation of pro-IL-1β and pro-IL-18 and the NLRP3 protein.

    “In these circumstances, ATP may act as DAMP, which activates the nuclear transcription factor NF-κB resulting in expression upregulation of pro-IL-1β and pro-IL-18 and the NLRP3 protein [16, 71].”
  • Consequently, there is an activation of caspase-1 and maturation of IL-1β and IL-18, resulting in pro-inflammatory cytokine release.

    “Consequently, there is an activation of caspase-1 and maturation of IL-1β and IL-18, resulting in pro-inflammatory cytokine release [16, 20, 52, 71, 73].”

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Authors
Jo, E.-K., Kim, J. K., Shin, D.-M., & Sasakawa, C.
Affiliations
  • Chungnam National University (KR)
  • Chiba University (JP)
Corresponding author
Jo, Eun-Kyeong
Venue
Cellular & Molecular Immunology
Published
2015-11-09
Volume
13
Issue
2
Pages
148-159
ISSN
  • 1672-7681 (ISSN-L)
  • 2042-0226
OpenAlex
W2118918019
Cited by
1,378
References
139
Citations by year
2026: 127 · 2025: 125 · 2024: 157 · 2023: 162 · 2022: 145 · 2021: 173 · 2020: 171 · 2019: 122 · 2018: 97 · 2017: 61 · 2016: 36
FWCI
6.27
Type
journal article
Language
en
Open access
Locations
  • Cellular and Molecular Immunology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
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, autoinflammatory disease, autoimmune disease, anti-inflammatory therapy, inflammasome assembly, inflammatory diseases
MeSH terms
NLR Family, Pyrin Domain-Containing 3 Protein, Animals, Autoimmune Diseases, Cytosol, Humans, Inflammation, Signal Transduction, Interleukin-1beta, Inflammasomes

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