Abstract: Behçet syndrome (BS) is a chronic, relapsing, multisystem inflammatory disorder in which both innate and adaptive immune mechanisms contribute to disease pathogenesis. Among innate immune cells, neutrophils have emerged as key effectors driving tissue inflammation, endothelial injury, and immunothrombosis. Early studies demonstrated enhanced chemotaxis, oxidative burst, and a primed activation state of circulating neutrophils, whereas more recent evidence highlights excessive neutrophil extracellular trap (NET) formation as an important contributor to vascular inflammation and thrombosis. In addition, recent omics-based studies have provided novel insights into neutrophil heterogeneity, activation pathways, and disease-specific signatures in BS. This review summarizes current knowledge on the role of neutrophils and NETs in the pathogenesis of BS, summarizes available evidence on mechanisms of neutrophil activation, and highlights potential directions for future research. Keywords: Behçet syndrome, neutrophil, neutrophil extracellular traps, NET, oxidative burst, omics
Özgüler et al. (Fri,) studied this question.