A role for the tissue factor pathway in the pathogenesis of the antiphospholipid syndrome

The antiphospholipid syndrome (aPS) is a systemic autoimmune disorder that is characterised by laboratory markers of antiphospholipid antibodies (aPL) as well as clinical manifestations such as arterial and venous thrombosis, recurrent pregnancy loss and thrombocytopaenia. Although it is unclear precisely what mechanism(s) lead to thrombosis in aPS, it is probable that the contribution of aPL such as anti-β-2-glycoprotein-1 (anti- β2GP1) is significant. Indeed, there is increasing evidence that aPL may interfere with the tissue factor (TF) pathway of blood coagulation and its natural regulator tissue factor pathway inhibitor (TFPI), thus contributing toward the development of thrombosis in aPS. This paper will therefore review 1) the TF pathway of blood coagulation and TFPI, 2) clinical and laboratory aspects of aPL and aPS, and 3) interactions of aPL with the TF pathway, to highlight the potential significance of these in the pathogenesis of aPS