McNall-Knapp René Y
University of Oklahoma Health Sciences Center, Jimmy Everest Section of Pediatric Hematology/Oncology, University of Oklahoma Children's Physicians Building, Oklahoma City, OK 73104, USA.
Curr Rheumatol Rep. 2008 Jan;10(1):62-6. doi: 10.1007/s11926-008-0011-z.
Antiphospholipid antibodies (aPL) can cause thromboembolic events, but the reason for the thrombogenesis has not been fully elucidated. Studies show that the true pathogenic targets of aPL are plasma proteins involved in hemostasis (eg, beta(2)-glycoprotein I and prothrombin). These plasma proteins in turn bind to phospholipids, leading to the misclassification as "antiphospholipid" antibodies. The hemostatic system has abundant checks and balances to avoid excess hemorrhage and thrombosis. Thus, thrombosis requires more than interrupting one protein in the complex system. This review examines host genetic factors important in predisposition to thrombosis associated with aPL and concentrates on how antibodies in antiphospholipid syndrome interact with our natural anticoagulants and lead to thrombosis.
抗磷脂抗体（aPL）可引发血栓栓塞事件，但其血栓形成的原因尚未完全阐明。研究表明，aPL真正的致病靶点是参与止血的血浆蛋白（如β2糖蛋白I和凝血酶原）。这些血浆蛋白进而与磷脂结合，导致被错误归类为“抗磷脂”抗体。止血系统有丰富的制衡机制以避免过度出血和血栓形成。因此，血栓形成需要干扰复杂系统中的不止一种蛋白质。本综述探讨了在与aPL相关的血栓形成易感性中起重要作用的宿主遗传因素，并着重关注抗磷脂综合征中的抗体如何与我们的天然抗凝剂相互作用并导致血栓形成。
