产科抗磷脂综合征的发病机制:β2糖蛋白I的关键作用

P. Meroni, C. Grossi, F. Tedesco
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引用次数: 0

摘要

抗磷脂综合征(APS)是指与持续存在抗阴离子磷脂结合蛋白抗体相关的复发性妊娠发病率和/或血管血栓形成。β2糖蛋白I(β2GPI)和凝血酶原(PT)是通过功能性凝血[狼疮抗凝血剂(LA)]或固相分析[抗β2GPI依赖性心磷脂(aCL)和抗β2GPI]检测到的抗磷脂抗体(aPL)的主要抗原。β2GPI依赖性aPL是三种分类实验室标准阳性的原因。虽然针对β2GPI的中/高滴度抗体是APS血管和产科表现的危险因素,但持续的低滴度抗体也与妊娠并发症有关。来自aPL依赖性胎儿丢失的动物模型和体外系统的证据表明,β2GPI依赖性aPL可能具有致病性。在生理学上,β2GPI在胎盘水平上大量存在,可用于母体血液中循环的特异性抗体。一旦与蛋白质结合,抗体就会通过激活补体级联反应引发局部炎症,并影响滋养层和蜕膜功能。最后的结果是胎盘形成缺陷,而血栓事件显然不那么重要。β2GPI是一种多效性分子,对包括凋亡物质在内的多种分子具有清除作用,并表现出抗氧化活性。这些功能可能解释了β2GPI胎盘在组织重塑和低氧紧张区域的定位。由于β2GPI还与补体和凝血级联反应相互作用,其与特异性抗体的结合可能以多种方式影响胎盘形成的生理学。
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Pathogenesis of the obstetric antiphospholipid syndrome: the key role of beta 2 glycoprotein I
Antiphospholipid syndrome (APS) is defined by recurrent pregnancy morbidity and/or vascular thrombosis associated with the persistent presence of antibodies against anionic phospholipid-binding proteins. Beta 2 glycoprotein I (β2GPI) and prothrombin (PT) are the major antigens for antiphospholipid antibodies (aPL) detectable by functional coagulation [lupus anticoagulant (LA)] or solid-phase assays [anti-β2GPI-dependent cardiolipin (aCL) and anti-β2GPI]. β2GPI-dependent aPL are responsible for the positivity of the three classification laboratory criteria. While medium/high titers of antibodies against β2GPI are risk factors for both the vascular and the obstetric manifestations of APS, persistent low titers are also associated with pregnancy complications. There is evidence from animal models of aPL-dependent fetal loss and from in vitro systems that β2GPI-dependent aPL can be pathogenic. β2GPI is physiologically found in large quantities at the placental level being available for the specific antibodies circulating in the maternal blood. Once bound to the protein, the antibodies trigger a local inflammation via the activation of the complement cascade and affect trophoblast and decidual function. The final result is represented by defective placentation, while thrombotic events are apparently less important. β2GPI is a pleiotropic molecule with scavenging properties towards several molecules including apoptotic material and displays anti-oxidant activity. These functions may explain the β2GPI placental localization in an area of intensive tissue remodeling and low oxygen tension. Since β2GPI interacts also with the complement and the coagulation cascade, its binding with specific antibodies may affect the physiology of placentation in several ways.
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