New insights into the regulation of innate immunity by caspase-8

Vitaliya Sagulenko, Kate E. Lawlor, James E. Vince

Research output: Contribution to journalEditorialOtherpeer-review

10 Citations (Scopus)

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.

Original languageEnglish
Article number4
JournalArthritis Research & Therapy
Volume18
Issue number1
DOIs
Publication statusPublished - 13 Jan 2016
Externally publishedYes

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