Recruitment of pro-IL-1α to mitochondrial cardiolipin, via shared LC3 binding domain, inhibits mitophagy and drives maximal NLRP3 activation

Significance The NLRP3 inflammasome is a critical component of the innate immune response to infectious agents, but its overactivation is implicated in numerous pathologies, including atherosclerosis, Alzheimer’s Disease, gout, inflammatory bowel disease, and type 2 diabetes. Our study reveals a mechanism by which cells modulate NLRP3 inflammasome activation and identifies potential therapeutic targets to treat pathologies associated with NLRP3 inflammasome activation.