Multiple research groups have demonstrated that caspase-8 (CASP8)-mediated gasdermin D (GSDMD) cleavage drives pyroptotic cell death. Here, we discuss a novel role for the enzymatically inactive homolog of CASP8, the long isoform of cellular FLICE-like inhibitory protein (cFLIP_L), in the regulation of this process. Specifically, cFLIP-deficiency provides a model in which to study the mechanisms regulating CASP8-mediated activation of cell death and inflammatory signaling.

中文翻译：

---

从炎症到细胞死亡的转变。

多个研究小组已经证明，caspase-8 (CASP8) 介导的 gasdermin D (GSDMD) 裂解会导致细胞焦亡。在这里，我们讨论了 CASP8 的酶促失活同源物（细胞 FLICE 样抑制蛋白 (cFLIP _L )的长同种型）在调节该过程中的新作用。具体而言，cFLIP 缺陷提供了一个模型，可以在其中研究调节 CASP8 介导的细胞死亡和炎症信号传导激活的机制。