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dc.contributor.authorSagulenko, V
dc.contributor.authorLawlor, KE
dc.contributor.authorVince, JE
dc.date.accessioned2020-12-22T04:26:31Z
dc.date.available2020-12-22T04:26:31Z
dc.date.issued2016-01-13
dc.identifierpii: 10.1186/s13075-015-0910-0
dc.identifier.citationSagulenko, V., Lawlor, K. E. & Vince, J. E. (2016). New insights into the regulation of innate immunity by caspase-8. ARTHRITIS RESEARCH & THERAPY, 18 (1), https://doi.org/10.1186/s13075-015-0910-0.
dc.identifier.issn1478-6354
dc.identifier.urihttp://hdl.handle.net/11343/258069
dc.description.abstractCaspase-8 is required for extrinsic apoptosis, but is also central for preventing a pro-inflammatory receptor interacting protein kinase (RIPK) 3-mixed lineage kinase domain-like (MLKL)-dependent cell death pathway termed necroptosis. Despite these critical cellular functions, the impact of capase-8 deletion in the myeloid cell lineage, which forms the basis for innate immune responses, has remained unclear. In a recent article in Arthritis Research & Therapy, Cuda et al. report that myeloid cell-restricted caspase-8 loss leads to a very mild RIPK3-dependent inflammatory phenotype. The presented results suggest that inflammation does not arise exclusively because of RIPK3-mediated necroptotic death but that, in the absence of caspase-8, RIPK1 and RIPK3 enhance microbiome-driven Toll-like receptor-induced pro-inflammatory cytokine production.
dc.languageEnglish
dc.publisherBIOMED CENTRAL LTD
dc.titleNew insights into the regulation of innate immunity by caspase-8
dc.typeJournal Article
dc.identifier.doi10.1186/s13075-015-0910-0
melbourne.affiliation.departmentMedical Biology (W.E.H.I.)
melbourne.source.titleArthritis Research and Therapy
melbourne.source.volume18
melbourne.source.issue1
dc.rights.licenseCC BY
melbourne.elementsid1026933
melbourne.contributor.authorVince, James
melbourne.contributor.authorLawlor, Kathryn
dc.identifier.eissn1478-6362
melbourne.accessrightsOpen Access


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