Anti-phospholipid autoantibodies are a group of antibodies that can specifically bind to anionic phospholipids and phospholipid protein complexes. Recent studies have reported elevated serum anti-phospholipid autoantibody levels in patients with antiphospholipid syndrome, systemic lupus erythematosus, rheumatoid arthritis, metabolic disorders, malaria, SARS-CoV-2 infection, obstetric diseases and cardiovascular diseases. However, the underlying mechanisms of anti-phospholipid autoantibodies in disease pathogenesis remain largely unclear. Emerging evidence indicate that anti-phospholipid autoantibodies modulate NETs formation, monocyte activation, blockade of apoptotic cell phagocytosis in macrophages, complement activation, dendritic cell activation and vascular endothelial cell activation. Herein, we provide an update on recent advances in elucidating the effector mechanisms of anti-phospholipid autoantibodies in the pathogenesis of various diseases, which may facilitate the development of potential therapeutic targets for the treatment of anti-phospholipid autoantibody-related disorders.
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Laboratoire d'Immunologie, AP-HP, Hôpital Européen Georges Pompidou, Paris; and Inflammation, Complement, and Cancer, Université Paris Cité, INSERM, UMRS 1138, Cordeliers Research Center, Team Paris, France.
Objectives: Antiphospholipid syndrome (APS) is an autoimmune disease combining the occurrence of thrombotic and/or obstetric events with the persistent presence of antiphospholipid antibodies (i.e. lupus anticoagulant (LA), anti-cardiolipin (aCL) and anti-beta-2-glycoprotein I (aβ2GPI) antibodies).
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January 2025
Research Center on Thromboembolic Disorders and Antithrombotic Therapies, ASST Lariana, University of Insubria, Como, Italy. Electronic address:
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- The review included 1056 participants and found that low-dose acetylsalicylic acid (LDA) significantly reduced both arterial and venous thrombotic events compared to control groups without increasing major bleeding risks.
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