The pathogenic mechanisms for antiphospholipid antibodies (aPL)-mediated pregnancy loss

Antiphospholipid antibodies (aPL) may affect placental functions through several possible mechanisms. It is now well accepted that these mechanisms are not mutually exclusive and may play a role together or in different combination at different times of the pregnancy process. Thrombotic placental pathology was initially suggested as the main pathogenic event involved in the APS-related pregnancy morbidity. However histological analysis of abortive material or full-term placentae from women with APS was not able to support the thrombotic theory. It is now well documented that the most clinically relevant aPL, anti-β2 glycoprotein I antibodies (anti-β2GPI), can react with human trophoblast, decidual, and endometrial endothelial cells. Following their binding, anti-β2GPI are able to induce a direct damage on placental tissue, hence resulting in a defective placentation. A further mechanism by which aPL contribute to obstetric morbidity is their ability to activate the complement system. Numerous ameliorations in the knowledge of aPL pathogenic action have been introduced in the last few years. To have clarified the mechanisms of aPL-mediated damage on placental tissue has represented an important step allowing the introduction of new possible therapeutical possibilities able to abrogate the aPL pathogenic effect.