Antiphospholipid syndrome (APS) is an autoimmune thromboinflammatory disorder in which antiphospholipid antibodies cause vascular thrombosis and obstetric morbidity. Growing evidence indicates that neutrophils and monocytes are key effector cells bridging inflammation and coagulation in APS. Neutrophils display heightened activation, enhanced glycolysis, and exaggerated NETosis, with downstream neutrophil extracellular traps promoting endothelial injury, complement activation, and trophoblast dysfunction. Dysregulated purinergic signaling in APS neutrophils further amplifies thromboinflammatory crosstalk with platelets and the endothelium. Monocytes similarly exhibit proinflammatory skewing, manifesting as increased expression of adhesion molecules and robust induction of tissue factor. Epigenetic alterations in both neutrophils and monocytes may further prime their pathogenic activation. Together, these findings implicate neutrophils and monocytes as important mediators of immunothrombosis and highlight them as potential therapeutic targets in APS.
Yalavarthi et al. (Thu,) studied this question.