Show simple item record

dc.contributor.authorFeltham, R
dc.contributor.authorVince, JE
dc.contributor.authorLawlor, KE
dc.date.accessioned2020-12-22T04:09:19Z
dc.date.available2020-12-22T04:09:19Z
dc.date.issued2017-01-06
dc.identifier.citationFeltham, R., Vince, J. E. & Lawlor, K. E. (2017). Caspase-8: not so silently deadly. CLINICAL & TRANSLATIONAL IMMUNOLOGY, 6 (1), https://doi.org/10.1038/cti.2016.83.
dc.identifier.issn2050-0068
dc.identifier.urihttp://hdl.handle.net/11343/258007
dc.description.abstractApoptosis is a caspase-dependent programmed form of cell death, which is commonly believed to be an immunologically silent process, required for mammalian development and maintenance of cellular homoeostasis. In contrast, lytic forms of cell death, such as RIPK3- and MLKL-driven necroptosis, and caspase-1/11-dependent pyroptosis, are postulated to be inflammatory via the release of damage associated molecular patterns (DAMPs). Recently, the function of apoptotic caspase-8 has been extended to the negative regulation of necroptosis, the cleavage of inflammatory interleukin-1β (IL-1β) to its mature bioactive form, either directly or via the NLRP3 inflammasome, and the regulation of cytokine transcriptional responses. In view of these recent advances, human autoinflammatory diseases that are caused by mutations in cell death regulatory machinery are now associated with inappropriate inflammasome activation. In this review, we discuss the emerging crosstalk between cell death and innate immune cell inflammatory signalling, particularly focusing on novel non-apoptotic functions of caspase-8. We also highlight the growing number of autoinflammatory diseases that are associated with enhanced inflammasome function.
dc.languageEnglish
dc.publisherWILEY
dc.rights.urihttps://creativecommons.org/licenses/by/4.0
dc.titleCaspase-8: not so silently deadly
dc.typeJournal Article
dc.identifier.doi10.1038/cti.2016.83
melbourne.affiliation.departmentMedical Biology (W.E.H.I.)
melbourne.source.titleClinical & Translational Immunology
melbourne.source.volume6
melbourne.source.issue1
dc.rights.licenseCC BY
melbourne.elementsid1183741
melbourne.contributor.authorVince, James
melbourne.contributor.authorLawlor, Kathryn
melbourne.contributor.authorFeltham, Rebecca
dc.identifier.eissn2050-0068
melbourne.accessrightsOpen Access


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record