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 phosphatidylserine 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 phenomena, recurrent fetal loss and prolonged activated partial thromboplastin time (aPTT). In one patient the antiphosphatidylserine Abs were the main antiphospholipid antibody (aPL) while the 2nd patient also had pathogenic aCL. The purified antibodies were passively infused into the tail vein of mice. The mice were mated and we followed them for manifestations of APS.
RESULTS: Passive infusion of IgG but not IgM antiphosphatidylserine antibodies to pregnant ICR mice resulted in increased fetal resorption rate (40%), lower mean weights of the placentae and fetuses and prolonged aPTT (82 s). Antiphosphatidylserine antibodies were detected in the placentae.
CONCLUSIONS: Our results point to the pathogenic role of antiphosphatidylserine antibodies and emphasize the importance of looking for the presence of antiphosphatidylserine Abs in sera of patients with clinical manifestations compatible with APS even in the absence of aCL Abs.