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

TP Monie, CE Bryant - Immunological reviews, 2015 - Wiley Online Library
TP Monie, CE Bryant
Immunological reviews, 2015Wiley Online Library
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 RIPK 3‐
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 …
Summary
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.
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