The role of neutrophil extracellular traps in antiphospholipid syndrome

Antiphospholipid syndrome (APS) is an acquired systemic autoimmune disorder characterized clinically by recurrent arterial and venous thrombosis and/or adverse pregnancy outcomes, and laboratory-defined by persistently positive antiphospholipid antibodies (aPLs). Neutrophils are the most abundant white blood cells in the circulation. In APS patients, aPLs abnormally activate neutrophils, causing them to transition from a quiescent state to a highly activated state, which is a central mechanism in disease pathogenesis. Neutrophil extracellular traps (NETs) are reticular structures composed of DNA, histones, and granular proteins released by neutrophils under stress conditions. As a crucial immune mechanism for neutrophil function, NETs play a vital role in anti-infection and immune responses. However, when overactivated or lacking inhibition, NETs can mediate the development of various diseases. Recent studies indicate that neutrophils and NETs occupy a central position in APS pathogenesis, promoting thrombosis and contributing to pathological processes such as placental dysfunction. This review summarizes the role of NETs in the development and progression of APS.