TY  - JOUR
AU  - Sagulenko, V
AU  - Lawlor, KE
AU  - Vince, JE
Y2  - 2020/12/22
Y1  - 2016/01/13
SN  - 1478-6354
UR  - http://hdl.handle.net/11343/258069
AB  - 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.
LA  - English
PB  - BIOMED CENTRAL LTD
T1  - New insights into the regulation of innate immunity by caspase-8
DO  - 10.1186/s13075-015-0910-0
IS  - Arthritis Research and Therapy
VL  - 18
IS  - 1
L1  - /bitstream/handle/11343/258069/PMC4718034.pdf?sequence=1&isAllowed=y
ER  -