Secretion of the cytokine interleukin-1b (IL-1b) by macrophages, a major driver of pathogenesis in atherosclerosis, requires two steps: Priming signals promote transcription of immature IL-1b, and then endogenous "danger" signals activate innate immune signaling complexes called inflammasomes to process IL-1b for secretion. Although cholesterol crystals are known to act as danger signals in atherosclerosis, what primes IL-1b transcription remains elusive. Using a murine model of atherosclerosis, we found that cholesterol crystals acted both as priming and danger signals for IL-1b production. Cholesterol crystals triggered neutrophils to release neutrophil extracellular traps (NETs). NETs primed macrophages for cytokine release, activating T helper 17 (TH17) cells that amplify immune cell recruitment in atherosclerotic plaques. Therefore, danger signals may drive sterile inflammation, such as that seen in atherosclerosis, through their interactions with neutrophils.