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Antiphospholipid syndrome (APS) is characterised by arterial and/or venous thrombosis and recurrent fetal loss in association with the presence of antiphospholipid antibodies (aPL). In addition to β2-glycoprotein I, prothrombin (PT) is an important autoantigen recognised by aPL. PT is a coagulation proenzyme abundantly present in blood (70–100 μg/ml), and binds to negatively charged phospholipids such as phosphatidylserine. PT comprises two major domains, fragment-1 (F-1) and prethrombin-1 (Pre-1). We previously reported that antiprothrombin antibody (aPT) is a mixture of antibodies against both F-1 and Pre-1, and that there are significant clinical differences between anti-F-1 and anti-Pre-1.1,2
aPL, including aPT, are not mere serological markers of the disease, but are important players in the pathogenesis of APS. Therefore, antigen-specific immunosuppressive treatments, if developed, will help to prevent …