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Disruptions in endocytic traffic contribute to the activation of the NLRP3 inflammasome

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dc.contributor.authorMartín Sánchez, María Rosario Fátima
dc.contributor.authorLee, Bali
dc.contributor.authorHoyle, Christopher
dc.contributor.authorWellens, Rose
dc.contributor.authorGreen, Jack P.
dc.contributor.authorWilliams, Daniel M.
dc.contributor.authorMatchett, Billie J.
dc.contributor.authorSeoane, Paula I.
dc.contributor.authorBennett, Hayley
dc.contributor.authorAdamson, Antony
dc.contributor.authorLópez Castejón, Gloria
dc.contributor.authorLowe, Martin
dc.contributor.authorBrough, David
dc.contributor.departmentFarmacología
dc.date.accessioned2026-02-26T15:05:56Z
dc.date.available2026-02-26T15:05:56Z
dc.date.copyright© 2023 AAAS
dc.date.issued2023-02-21
dc.description.abstractInflammation driven by the NLRP3 inflammasome is coordinated through multiple signaling pathways and is regulated by sub-cellular organelles. Here, we tested the hypothesis that NLRP3 senses disrupted endosome trafficking to trigger inflammasome formation and inflammatory cytokine secretion. NLRP3-activating stimuli disrupted endosome trafficking and triggered localization of NLRP3 to vesicles positive for endolysosomal markers and for the inositol lipid PI4P. Chemical disruption of endosome trafficking sensitized macrophages to the NLRP3 activator imiquimod, driving enhanced inflammasome activation and cytokine secretion. Together, these data suggest that NLRP3 can sense disruptions in the trafficking of endosomal cargoes, which may explain in part the spatial activation of the NLRP3 inflammasome. These data highlight mechanisms that could be exploited in the therapeutic targeting of NLRP3.
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dc.identifier.citationScience Signaling, 2023, Vol 16, Issue 773
dc.identifier.doihttps://doi.org/10.1126/scisignal.abm7134
dc.identifier.eissn1937-9145
dc.identifier.issn1945-0877
dc.identifier.urihttp://hdl.handle.net/10201/214841
dc.languageeng
dc.publisherAmerican Association for the Advancement of Science
dc.relationEste trabajo ha sido financiado por: - Wellcome Trust (104192/Z/14/Z) - Medical Research Council (MR/T016515/1) - British Heart Foundation (AA/18/4/34221)
dc.relation.publisherversionhttps://www.science.org/doi/10.1126/scisignal.abm7134
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subject.odsObjetivo 3: Salud
dc.titleDisruptions in endocytic traffic contribute to the activation of the NLRP3 inflammasome
dc.typeinfo:eu-repo/semantics/article
dc.type.versioninfo:eu-repo/semantics/acceptedVersion
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relation.isAuthorOfPublicationeefc2e40-b110-47b5-a081-bcf37256af4c
relation.isAuthorOfPublication.latestForDiscoveryeefc2e40-b110-47b5-a081-bcf37256af4c
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