INDUCTION OF EXPERIMENTAL ANTIPHOSPHOLIPID SYNDROME IN NAIVE MICE WITH PURIFIED IGG ANTIPHOSPHATIDYLSERINE ANTIBODIES

Objective. It is accepted that antiphospholipid syndrome (APS) is due to the presence of anticardiolipin antibodies (aCL). Since phosphatidy lserine is a negatively charged phospholipid, we tried to demonstrate the pathogenic role of antiphosphatidylserine in APS. Methods. We used affinity purified IgG antiphosphatidylserine antibodies from sera of 2 patients with APS characterized by recurrent thromboembolic phenomen a, recurrent fetal loss and prolonged activated partial thromboplastin time (aPTT). In one patient the antiphosphatidylserine Abs were the m ain antiphospholipid antibody (aPL) while the 2nd patient also had pat hogenic aCL. The purified antibodies were passively infused into the t ail vein of mice. The mice were mated and we followed them for manifes tations of APS. Results. Passive infusion of IgG but not IgM antiphosp hatidylserine antibodies to pregnant ICR mice resulted in increased fe tal resorption rate (40%), lower mean weights of the placentae and fet uses and prolonged aPTT (82 s). Antiphosphatidylserine antibodies were detected in the placentae. Conclusions. Our results point to the path ogenic role of antiphosphatidylserine antibodies and emphasize the imp ortance of looking for the presence of antiphosphatidylserine Abs in s era of patients with clinical manifestations compatible with APS even in the absence of aCL Abs.