D'Ippolito Silvia, Di Simone Nicoletta, Di Nicuolo Fiorella, Castellani Roberta, Caruso Alessandro
Department of Obstetrics and Gynecology, Catholic University of Sacred Heart, Rome, Italy.
Am J Reprod Immunol. 2007 Aug;58(2):150-8. doi: 10.1111/j.1600-0897.2007.00500.x.
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.
An analysis of published data.
It is now generally accepted that the clinically relevant aPL bind to proteins with affinity for phospholipids (PL), such as beta2-glycoprotein I (beta2-GPI). Following the attachment of beta2-GPI to trophoblast anionic PL, both molecules undergo conformational changes resulting in the exposure of cryptic epitopes within the structure of beta2-GPI. This may allow the subsequent binding of antibodies hence affecting trophoblast functions directly. Moreover anti-beta2-GPI antibodies induce the activation of endothelial cells (ECs), resulting in a proinflammatory state which favours the prothrombotic diathesis of the syndrome.
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.
抗磷脂综合征（APS）可能通过多种潜在机制影响胎盘功能。抗磷脂抗体（aPL）与参与凝血级联反应的细胞相互作用被认为会导致促凝状态。然而，血栓形成性胎盘病理改变并非APS所特有。
对已发表数据进行分析。
目前普遍认为，具有临床相关性的aPL与对磷脂（PL）具有亲和力的蛋白质结合，如β2-糖蛋白I（β2-GPI）。β2-GPI附着于滋养层阴离子磷脂后，两个分子都会发生构象变化，导致β2-GPI结构内隐蔽表位暴露。这可能会使抗体随后结合，从而直接影响滋养层功能。此外，抗β2-GPI抗体可诱导内皮细胞（ECs）活化，导致促炎状态，这有利于该综合征的血栓形成倾向。
在过去几年中，人们对APS的认识有了许多改进。阐明抗体介导的对滋养层和内皮细胞的损伤机制是解释导致妊娠并发症的细胞事件的重要一步。
