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Cell death is not essential for caspase-1-mediated interleukin-1β activation and secretion

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dc.contributor.authorConos, S.A.
dc.contributor.authorLawlor, K.E.
dc.contributor.authorVaux, D.L.
dc.contributor.authorVince, J.E.
dc.contributor.authorLindqvist, L.M.
dc.date.issued2016
dc.descriptionData source: Supplementary information, https://doi.org/10.1038/cdd.2016.69 Link to a related website: http://europepmc.org/articles/pmc5071572?pdf=render, Open Access via Unpaywall
dc.description.abstractCaspase-1 cleaves and activates the pro-inflammatory cytokine interleukin-1β (IL-1β), yet the mechanism of IL-1β release and its dependence on cell death remains controversial. To address this issue, we generated a novel inflammasome independent system in which we directly activate caspase-1 by dimerization. In this system, caspase-1 dimerization induced the cleavage and secretion of IL-1β, which did not require processing of caspase-1 into its p20 and p10 subunits. Moreover, direct caspase-1 dimerization allowed caspase-1 activation of IL-1β to be separated from cell death. Specifically, we demonstrate at the single cell level that IL-1β can be released from live, metabolically active, cells following caspase-1 activation. In addition, we show that dimerized or endogenous caspase-8 can also directly cleave IL-1β into its biologically active form, in the absence of canonical inflammasome components. Therefore, cell death is not obligatory for the robust secretion of bioactive IL-1β.
dc.identifier.citationCell Death and Differentiation, 2016; 23(11):1827-1838
dc.identifier.doi10.1038/cdd.2016.69
dc.identifier.issn1350-9047
dc.identifier.issn1476-5403
dc.identifier.urihttps://hdl.handle.net/11541.2/131452
dc.language.isoen
dc.publisherNature Publishing Group
dc.relation.fundingNHMRC 1051210
dc.relation.fundingNHMRC 1101405
dc.relation.fundingNHMRC 1052598
dc.relation.fundingNHMRC 1035502
dc.relation.fundingNHMRC 1020136
dc.relation.fundingNHMRC 461221
dc.relation.fundingVictorian State Government OIS 361646
dc.relation.fundingAustralian Government IRISS
dc.rightsCopyright 2016 Springer Nature
dc.source.urihttps://doi.org/10.1038/cdd.2016.69
dc.subjectinflammasome
dc.subjectinterleukins
dc.subjectcytokine
dc.subjectcell death
dc.subjectimmune response
dc.titleCell death is not essential for caspase-1-mediated interleukin-1β activation and secretion
dc.typeJournal article
pubs.publication-statusPublished
ror.mmsid9916178483301831

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