Cholesterol crystals trigger neutrophil extracellular traps (NETs) to prime macrophages for cytokine production, particularly interleukin-1β (IL-1β), in atherosclerosis. NETs, composed of decondensed chromatin and antimicrobials, are released by neutrophils in response to cholesterol crystals. These NETs activate macrophages and Th17 cells, leading to increased cytokine production and immune cell recruitment in atherosclerotic plaques. The study demonstrates that NETs play a crucial role in driving sterile inflammation in atherosclerosis by modulating cytokine production and promoting a self-amplifying IL-1/IL-17 cascade.Cholesterol crystals trigger neutrophil extracellular traps (NETs) to prime macrophages for cytokine production, particularly interleukin-1β (IL-1β), in atherosclerosis. NETs, composed of decondensed chromatin and antimicrobials, are released by neutrophils in response to cholesterol crystals. These NETs activate macrophages and Th17 cells, leading to increased cytokine production and immune cell recruitment in atherosclerotic plaques. The study demonstrates that NETs play a crucial role in driving sterile inflammation in atherosclerosis by modulating cytokine production and promoting a self-amplifying IL-1/IL-17 cascade.