Caspase-8: not so silently deadly
- Author(s)
- Feltham, R; Vince, JE; Lawlor, KE;
- Details
- Publication Year 2017-01,Volume 6,Issue #1,Page e124
- Journal Title
- Clin Transl Immunology
- Publication Type
- Journal Article
- Abstract
- Apoptosis 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-1beta (IL-1beta) 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.
- Publisher
- ASI
- Research Division(s)
- Inflammation
- PubMed ID
- 28197335
- Publisher's Version
- https://doi.org/10.1038/cti.2016.83
- Open Access at Publisher's Site
http://www.nature.com/cti/journal/v6/n1/full/cti201683a.html- NHMRC Grants
- NHMRC/1101405, NHMRC/1081272, NHMRC/1052598,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2017-04-06 09:27:49
Last Modified: 2017-04-10 12:35:07