2025 Volume 74 Issue 4 Pages 680-686
Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the presence of antiphospholipid antibody (aPL), which is autoantibody targeting phospholipid-related proteins in the blood. This condition leads to complications such as arterial and venous thrombosis and recurrent pregnancy loss. In Japan, approximately half of APS cases are secondary APS associated with autoimmune diseases, the most common being systemic lupus erythematosus (SLE). APS in conjunction with SLE (SLE/APS) is known to cause severe and diverse thrombotic events, though the underlying pathophysiological mechanisms remain unclear. Recent studies have suggested that excessive formation of neutrophil extracellular traps (NETs) is a major mechanism contributing to thrombosis in APS and SLE/APS. This study aimed to elucidate the impact of aPL on NETs formation. Human peripheral blood granulocytes were stimulated with serum from SLE/APS patients and aPL IgG to examine whether NET formation is induced. The results indicated that aPL could potentially induce an increase in the proportion of SYTOX® Green-positive cells, neutrophil elastase activity in culture supernatants, and the proportion of reactive oxygen species (ROS)-producing cells within granulocytes. These findings suggest that aPL-induced cell death is associated with NETs formation. Furthermore, they imply that in the blood of APS patients, aPL may promote thrombosis through NETs.
