Antiphospholipid antibodies provide a model for immune-mediated thrombosis. Study of the pathophysiological effects of antiphospholipid antibodies has revealed several potential thrombotic mechanisms. Experiments designed to elucidate these mechanisms have used both in vitro and in vivo techniques. Results implicate endothelial anticoagulant dysfunction, abnormalities of prostacyclin, antithrombin III, placental anticoagulant protein, proteins C and S, and complement activation, any of which could lead to thrombosis. In an individual patient, thrombosis may result from a combination of these abnormalities or it may require the presence of other nonimmune-mediated perturbations of the coagulation system.