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The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.

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Title: The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.
Authors: Xiao N; Department of Microbiology, University of Chicago, Chicago, IL, USA., Lu Z; Department of Microbiology, University of Chicago, Chicago, IL, USA., Cooper DK; Department of Microbiology, University of Chicago, Chicago, IL, USA., Chen J; Department of Microbiology, University of Chicago, Chicago, IL, USA. jueqi@uchicago.edu.; Howard Taylor Ricketts Laboratory, University of Chicago, Lemont, IL, USA. jueqi@uchicago.edu.
Source: Cellular & molecular immunology [Cell Mol Immunol] 2026 Oct; Vol. 23 (10), pp. 1194-1218. Date of Electronic Publication: 2026 Sep 02.
Publication Type: Journal Article; Review
Language: English
Journal Info: Publisher: Chinese Society of Immunology Country of Publication: China NLM ID: 101242872 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2042-0226 (Electronic) Linking ISSN: 16727681 NLM ISO Abbreviation: Cell Mol Immunol Subsets: MEDLINE
Imprint Name(s): Original Publication: Beijing, China : Tokyo, Japan : Chinese Society of Immunology; Nature Pub. Group, 2010-
MeSH Terms: Inflammasomes*/metabolism , Inflammasomes*/immunology , NLR Family, Pyrin Domain-Containing 3 Protein*/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein*/immunology , Immunity, Innate* , Signal Transduction*, Inflammation/immunology ; Humans ; Animals ; Cell Death ; Innate Immunity Recognition ; cGAS-STING Signaling Pathway
Abstract: The NLRP3 inflammasome is a central signaling pathway of innate immunity that orchestrates host defense and inflammatory responses through the activation of proinflammatory cytokines and the induction of pyroptotic cell death. Accumulating evidence indicates that NLRP3 functions within an extensive network of innate immune and cell death pathways. Reciprocal interactions between NLRP3 and other pattern-recognition receptor pathways, including Toll-like receptors, DNA-sensing cGAS-STING signaling, and RNA-sensing RIG-I/MDA5-MAVS signaling, shape the magnitude and duration of inflammatory responses during pathogen infection. Moreover, substantial crosstalk exists between NLRP3 and other inflammasomes and programmed cell death pathways, reflecting the integrated nature of cellular stress and inflammatory signaling. In this review, we summarize recent advances in our understanding of the molecular mechanisms that mediate these interactions, focusing on shared signaling components, organelle dynamics, posttranslational modifications, and feedback regulatory circuits. We further discuss how these signaling networks contribute to infectious and inflammatory diseases and highlight key unanswered questions and emerging areas of investigation that may guide the development of therapies targeting inflammasome-associated pathologies.
(© 2026. The Author(s).)
Competing Interests: Competing interests: The authors declare no competing interests.
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Grant Information: R35 GM151390 United States GM NIGMS NIH HHS; R35GM151390 U.S. Department of Health & Human Services | National Institutes of Health (NIH)
Contributed Indexing: Keywords: Cell death; Inflammasome; Innate immunity
Substance Nomenclature: 0 (Inflammasomes)
0 (NLR Family, Pyrin Domain-Containing 3 Protein)
Entry Date(s): Date Created: 20260903 Date Completed: 20260929 Latest Revision: 20261008
Update Code: 20261008
PubMed Central ID: PMC13623877
DOI: 10.1038/s41423-026-01463-2
PMID: 42687020
Database: MEDLINE
FullText Text:
  Availability: 0
Header DbId: cmedm
DbLabel: MEDLINE
An: 42687020
AccessLevel: 3
PubType: Academic Journal
PubTypeId: academicJournal
PreciseRelevancyScore: 0
IllustrationInfo
Items – Name: Title
  Label: Title
  Group: Ti
  Data: The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.
– Name: Author
  Label: Authors
  Group: Au
  Data: <searchLink fieldCode="AU" term="%22Xiao+N%22">Xiao N</searchLink>; Department of Microbiology, University of Chicago, Chicago, IL, USA.<br /><searchLink fieldCode="AU" term="%22Lu+Z%22">Lu Z</searchLink>; Department of Microbiology, University of Chicago, Chicago, IL, USA.<br /><searchLink fieldCode="AU" term="%22Cooper+DK%22">Cooper DK</searchLink>; Department of Microbiology, University of Chicago, Chicago, IL, USA.<br /><searchLink fieldCode="AU" term="%22Chen+J%22">Chen J</searchLink>; Department of Microbiology, University of Chicago, Chicago, IL, USA. jueqi@uchicago.edu.; Howard Taylor Ricketts Laboratory, University of Chicago, Lemont, IL, USA. jueqi@uchicago.edu.
– Name: TitleSource
  Label: Source
  Group: Src
  Data: <searchLink fieldCode="JN" term="%22101242872%22">Cellular & molecular immunology</searchLink> [Cell Mol Immunol] 2026 Oct; Vol. 23 (10), pp. 1194-1218. <i>Date of Electronic Publication: </i>2026 Sep 02.
– Name: TypePub
  Label: Publication Type
  Group: TypPub
  Data: Journal Article; Review
– Name: Language
  Label: Language
  Group: Lang
  Data: English
– Name: TitleSource
  Label: Journal Info
  Group: Src
  Data: <i>Publisher: </i><searchLink fieldCode="PB" term="%22Chinese+Society+of+Immunology%22">Chinese Society of Immunology </searchLink><i>Country of Publication: </i>China <i>NLM ID: </i>101242872 <i>Publication Model: </i>Print-Electronic <i>Cited Medium: </i>Internet <i>ISSN: </i>2042-0226 (Electronic) <i>Linking ISSN: </i><searchLink fieldCode="IS" term="%2216727681%22">16727681 </searchLink><i>NLM ISO Abbreviation: </i>Cell Mol Immunol <i>Subsets: </i>MEDLINE
– Name: PublisherInfo
  Label: Imprint Name(s)
  Group: PubInfo
  Data: <i>Original Publication</i>: Beijing, China : Tokyo, Japan : Chinese Society of Immunology; Nature Pub. Group, 2010-
– Name: SubjectMESH
  Label: MeSH Terms
  Group: Su
  Data: <searchLink fieldCode="MM" term="%22Inflammasomes%22">Inflammasomes*</searchLink>/<searchLink fieldCode="MM" term="%22Inflammasomes+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22Inflammasomes%22">Inflammasomes*</searchLink>/<searchLink fieldCode="MM" term="%22Inflammasomes+immunology%22">immunology</searchLink> <br /><searchLink fieldCode="MM" term="%22NLR+Family%2C+Pyrin+Domain-Containing+3+Protein%22">NLR Family, Pyrin Domain-Containing 3 Protein*</searchLink>/<searchLink fieldCode="MM" term="%22NLR+Family%2C+Pyrin+Domain-Containing+3+Protein+metabolism%22">metabolism</searchLink> <br /><searchLink fieldCode="MM" term="%22NLR+Family%2C+Pyrin+Domain-Containing+3+Protein%22">NLR Family, Pyrin Domain-Containing 3 Protein*</searchLink>/<searchLink fieldCode="MM" term="%22NLR+Family%2C+Pyrin+Domain-Containing+3+Protein+immunology%22">immunology</searchLink> <br /><searchLink fieldCode="MM" term="%22Immunity%2C+Innate%22">Immunity, Innate*</searchLink> <br /><searchLink fieldCode="MM" term="%22Signal+Transduction%22">Signal Transduction*</searchLink><br /><searchLink fieldCode="MH" term="%22Inflammation%22">Inflammation</searchLink>/<searchLink fieldCode="MH" term="%22Inflammation+immunology%22">immunology</searchLink> ; <searchLink fieldCode="MH" term="%22Humans%22">Humans</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Cell+Death%22">Cell Death</searchLink> ; <searchLink fieldCode="MH" term="%22Innate+Immunity+Recognition%22">Innate Immunity Recognition</searchLink> ; <searchLink fieldCode="MH" term="%22cGAS-STING+Signaling+Pathway%22">cGAS-STING Signaling Pathway</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: The NLRP3 inflammasome is a central signaling pathway of innate immunity that orchestrates host defense and inflammatory responses through the activation of proinflammatory cytokines and the induction of pyroptotic cell death. Accumulating evidence indicates that NLRP3 functions within an extensive network of innate immune and cell death pathways. Reciprocal interactions between NLRP3 and other pattern-recognition receptor pathways, including Toll-like receptors, DNA-sensing cGAS-STING signaling, and RNA-sensing RIG-I/MDA5-MAVS signaling, shape the magnitude and duration of inflammatory responses during pathogen infection. Moreover, substantial crosstalk exists between NLRP3 and other inflammasomes and programmed cell death pathways, reflecting the integrated nature of cellular stress and inflammatory signaling. In this review, we summarize recent advances in our understanding of the molecular mechanisms that mediate these interactions, focusing on shared signaling components, organelle dynamics, posttranslational modifications, and feedback regulatory circuits. We further discuss how these signaling networks contribute to infectious and inflammatory diseases and highlight key unanswered questions and emerging areas of investigation that may guide the development of therapies targeting inflammasome-associated pathologies.<br /> (© 2026. The Author(s).)
– Name: Abstract
  Label: Competing Interests
  Group: Ab
  Data: Competing interests: The authors declare no competing interests.
– Name: Ref
  Label: References
  Group: RefInfo
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  Data: R35 GM151390 United States GM NIGMS NIH HHS; R35GM151390 U.S. Department of Health & Human Services | National Institutes of Health (NIH)
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  Data: <i>Keywords: </i>Cell death; Inflammasome; Innate immunity
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  Data: <i>Date Created: </i>20260903 <i>Date Completed: </i>20260929 <i>Latest Revision: </i>20261008
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        Value: 10.1038/s41423-026-01463-2
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      – Code: eng
        Text: English
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        StartPage: 1194
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      – SubjectFull: Inflammation immunology
        Type: general
      – SubjectFull: Humans
        Type: general
      – SubjectFull: Animals
        Type: general
      – SubjectFull: Cell Death
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      – SubjectFull: Innate Immunity Recognition
        Type: general
      – SubjectFull: cGAS-STING Signaling Pathway
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      – SubjectFull: Inflammasomes metabolism
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      – SubjectFull: Inflammasomes immunology
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      – SubjectFull: NLR Family, Pyrin Domain-Containing 3 Protein metabolism
        Type: general
      – SubjectFull: NLR Family, Pyrin Domain-Containing 3 Protein immunology
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      – SubjectFull: Immunity, Innate
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      – SubjectFull: Signal Transduction
        Type: general
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      – TitleFull: The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.
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            – D: 01
              M: 10
              Text: 2026 Oct
              Type: published
              Y: 2026
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              Value: 2042-0226
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              Value: 23
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              Value: 10
          Titles:
            – TitleFull: Cellular & molecular immunology
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