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

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.
Συγγραφείς: 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.
Πηγή: Cellular & molecular immunology [Cell Mol Immunol] 2026 Oct; Vol. 23 (10), pp. 1194-1218. Date of Electronic Publication: 2026 Sep 02.
Τύπος έκδοσης: Journal Article; Review
Γλώσσα: English
Στοιχεία περιοδικού: 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-
Ιατρικοί όροι (MeSH): 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
Περίληψη: 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
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:2042-0226
DOI:10.1038/s41423-026-01463-2