Role of monocytes in the pathogenesis of antiphospholipid syndrome and potential therapeutic targets (Review).

Abstract

Antiphospholipid syndrome (APS) is an autoimmune disorder characterized primarily by arterial and/or venous thrombosis, obstetric complications and persistent positivity for antiphospholipid antibodies (aPLs). It has been proposed that the pathogenesis of APS is closely associated with vascular endothelial cell activation, complement activation and platelet activation. Notably, APS may be key to understanding the relationship between innate immune cells, and thrombosis and obstetric complications. Monocytes are activated by aPLs, adopting a pro‑inflammatory and pro‑coagulant phenotype, and producing inflammatory cytokines; however, the exact mechanisms of action of monocytes in APS remain unclear. Monocytes may act as an intermediary, triggering immune dysregulation, closely linking them to thrombosis and obstetric complications. Therefore, a better understanding of the potential pathogenic role of monocytes in APS is required, which could assist clinicians in gaining deeper insights into the pathogenesis of APS and identifying new therapeutic targets. This may provide new options for the management of APS. Therefore, the present study aimed to review monocytes and their role in APS.