Problem Antiphospholipid syndrome (APS) may affect placental functions through several possible mechanisms. Interaction of antiphospholipid antibodies (aPL) with cells involved in the coagulation cascade is thought to produce a procoagulant state. Thrombotic placental pathology is however not specific for the APS.
Method of study An analysis of published data.
Results It is now generally accepted that the clinically relevant aPL bind to proteins with affinity for phospholipids (PL), such as β2-glycoprotein I (β2-GPI). Following the attachment of β2-GPI to trophoblast anionic PL, both molecules undergo conformational changes resulting in the exposure of cryptic epitopes within the structure of β2-GPI. This may allow the subsequent binding of antibodies hence affecting trophoblast functions directly.
Moreover anti-β2-GPI antibodies induce the activation of endothelial cells (ECs), resulting in a proinflammatory state which favours the prothrombotic diathesis of the syndrome.
Conclusion Numerous ameliorations in the APS knowledge have been introduced in the last few years. To have clarified the mechanism of antibody mediated damage on trophoblast and ECs represents an important step to explain the cellular events leading to pregnancy complications.