Description:
<jats:title>Summary</jats:title><jats:p>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 <jats:styled-content style="fixed-case">RIPK</jats:styled-content>3‐driven necroptosis. Genetic deletion of <jats:italic>Casp8</jats:italic> results in embryonic lethality as a result of uncontrolled necroptosis. This lethality can be rescued by simultaneous deletion of <jats:italic>Ripk3</jats:italic>. 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‐<jats:styled-content style="fixed-case">IL</jats:styled-content>‐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.</jats:p>