Thrombotic Risk of Neutrophil Extracellular Traps and Contact System in Patients with Antiphospholipid Antibodies

APAs) and an increased risk of thrombosis [1].In thrombosis, APAs may contribute through the induction of tissue factor expression in endothelial cells and platelet activation.However, the exact mechanisms underlying thrombosis in APS remain unclear.Upon stimulation by microorganisms, neutrophils release their nuclear contents into the extracellular space, forming structures known as neutrophil extracellular traps (NETs), which inhibit bacterial dissemination.In addition to microorganisms, NET formation can be triggered by various stimuli, including autoantibodies, cytokines, and cholesterol [1].Because APAs have been shown to induce NET formation in both in vitro[2] and in vivo mouse experiments [3], APA-induced NET formation has received considerable attention as a potential pathogenic mechanism in APS [4].Released NET contents are primarily composed of double-stranded DNA (dsDNA), histones, neutrophil elastase, and myeloperoxidase.These components can be recognized as autoantigens by the host immune system, thereby triggering a vicious cycle of au-BODY Antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of antiphospholipid antibodies 항인지질 항체 양성 환자에서 호중구 세포외 트랩 및 접촉계의 혈전 형성 위험 Thrombotic Risk of Neutrophil Extracellular Traps and Contact System in Patients with Antiphospholipid Antibodies