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Caspase-8 functions as a key mediator of inflammation and pro-IL-1β processing via both canonical and non-canonical pathways.


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Authors

Monie, Tom P 
Bryant, Clare E 

Abstract

Caspase-8 is an apical component of cell death pathways. Activated caspase-8 can drive classical caspase-dependent apoptosis and actively inhibits cell death mediated by RIPK3-driven necroptosis. Genetic deletion of Casp8 results in embryonic lethality as a result of uncontrolled necroptosis. This lethality can be rescued by simultaneous deletion of Ripk3. Recently, caspase-8 has been additionally connected to inflammatory pathways within the cell. In particular, caspase-8 has been shown to be crucially involved in the induction of pro-IL-1β synthesis and processing via both non-canonical and canonical pathways. In this review, we bring together current knowledge regarding the role of caspase-8 in cellular inflammation with a particular emphasis on the interplay between caspase-8 and the classical and non-canonical inflammasomes.

Description

Keywords

apoptosis, caspase, death receptor, inflammasome, interleukin-1β, signal transduction, Animals, Caspase 8, Cell Death, Humans, Inflammasomes, Inflammation, Interleukin-1beta, Receptor-Interacting Protein Serine-Threonine Kinases, Signal Transduction

Journal Title

Immunol Rev

Conference Name

Journal ISSN

0105-2896
1600-065X

Volume Title

265

Publisher

Wiley
Sponsorship
Biotechnology and Biological Sciences Research Council (BB/K006436/1)
Biotechnology and Biological Sciences Research Council (BB/H003916/1)
Wellcome Trust (108045/Z/15/Z)
The authors received financial support of the Wellcome Trust (TPM; WT085090MA) and the Biotechnology and Biological Sciences Research Council (CEB; BB/K006436/1).