Nobuhiko Kayagaki

TL;DR: This work suggests that MCC950/CRID3-based therapies may effectively treat inflammation driven by wild-type NLRP3 but notCAPS-associated mutants, and shows that CAPS-relatedNLRP3 mutants escape efficient MCC 950/ CRID3 inhibition.

TL;DR: It is shown that TRAIL/Apo2L suppresses autoimmune damage in relapsing‐remitting, and non-remitting models of experimental autoimmune encephalomyelitis (EAE), the first to illustrate the potential therapeutic value of recombinant TRAil/A po2L in suppressing T‐cell‐mediated autoimmune diseases.

TL;DR: The potential benefits of limiting membrane rupture rather than cell death by targeting NINJ1 and GSDMD were discussed in this paper, focusing on the targets of RIPK1 (receptor interacting serine/threonine kinase 1), NLRP3 (NLR family pyrin domain containing 3), and gSDMD (gasdermin D) as important mediators of lytic cell death.

TL;DR: The burgeoning caspase‐11‐dependent non‐canonical inflammasome field is reviewed, focusing mainly on the innate sensing of LPS, the major component of the outer membrane of Gram‐negative bacteria.

TL;DR: In this paper, the Shigella ubiquitin ligase IpaH7.8 functions as an inhibitor of GSDMD, and infection of human epithelial cells with IPAH 7.8-deficient shigella flexneri results in increased GSDmd-dependent cell death compared with wild type.