Jingjin Ding

TL;DR: It is demonstrated that the liposome-leakage and pore-forming activities of the gasdermin-N domain are required for pyroptosis and provide insights into the roles of theGasdermin family in necrosis, immunity and diseases.

TL;DR: It is shown that human monocytes, epithelial cells and keratinocytes undergo necrosis upon cytoplasmic delivery of LPS, which represents a new mode of pattern recognition in immunity and also an unprecedented means of caspase activation.

TL;DR: It is shown that GSDME, which was originally identified as DFNA5 (deafness, autosomal dominant 5), can switch caspase-3-mediated apoptosis induced by TNF or chemotherapy drugs to pyroptosis, suggesting that casp enzyme activation can trigger necrosis by cleaving G SDME and offer new insights into cancer chemotherapy.

TL;DR: It is shown that granzyme A cleaves and activates gasdermin B (GSDMB), a central player in the highly inflammatory cell death process known as pyroptosis, suggesting that this pathway may be a target for future cancer immunotherapies.

TL;DR: In mouse models of cancer, a biorthogonal chemical system based on desilylation catalysed by phenylalanine trifluoroborate enables the controlled release of gasdermin to induce pyroptosis selectively in tumour cells, suggesting that pyroPTosis-induced inflammation triggers robust antitumour immunity and can synergize with checkpoint blockade.