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

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.

• Authors: Tom P Monie, Clare E Bryant
• Journal: Immunological reviews (Immunol Rev) Vol. 265 Issue 1 Pg. 181-93 (May 2015) ISSN: 1600-065X [Electronic] England
• PMID: 25879293 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
• Copyright: © 2015 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Chemical References

• Inflammasomes
• Interleukin-1beta
• RIPK3 protein, human
• Receptor-Interacting Protein Serine-Threonine Kinases
• Caspase 8

Topics

• Animals
• Caspase 8 (genetics, metabolism)
• Cell Death
• Humans
• Inflammasomes (immunology, metabolism)
• Inflammation (metabolism)
• Interleukin-1beta (metabolism)
• Receptor-Interacting Protein Serine-Threonine Kinases (metabolism)
• Signal Transduction