New insights into the regulation of innate immunity by caspase-8
- Author(s)
- Sagulenko, V; Lawlor, KE; Vince, JE;
- Details
- Publication Year 2016,Volume 18,Issue #1,Page 4
- Journal Title
- Arthritis Res Ther
- Publication Type
- Journal Article
- Abstract
- Caspase-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.
- Publisher
- BioMed Central
- Research Division(s)
- Inflammation
- PubMed ID
- 26757916
- Publisher's Version
- https://doi.org/10.1186/s13075-015-0910-0
- NHMRC Grants
- NHMRC/1052598, NHMRC/1051210, NHMRC/1050651,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2016-01-29 11:46:09
Last Modified: 2016-01-29 01:56:36