Hanly J G, Hong C, Issekutz A
Department of Medicine, Dalhousie University, Halifax, Canada.
J Rheumatol. 1996 Sep;23(9):1543-9.
To examine beta 2-glycoprotein I (beta 2-GPI) binding and its ability to augment IgG anticardiolipin (aCL) antibody binding to resting and cytokine activated endothelial cells in vitro. To evaluate the ability of IgG aCL antibody positive sera to induce endothelial cell activation in vitro.
IgG with aCL activity was isolated by affinity purification from 6 patients with systemic lupus erythematosus (SLE) and 3 patients with primary antiphospholipid antibody syndrome (APS). Human umbilical vein endothelial cells (HUVEC) were cultured in serum-free conditions and examined in a resting state or after activation with tumor necrosis factor alpha (TNF-alpha). HUVEC were exposed to beta 2-GPI alone, IgG alone or IgG plus beta 2-GPI. Finally, we examined the ability of sera from the same patients with SLE and primary APS to activate HUVEC in culture.
Neither beta 2-GPI, IgG aCL, nor IgG aCL plus beta 2-GPI bound to resting or cytokine activated endothelial cells. In addition, sera from the same patients did not induce in vitro activation of endothelial cells as assessed by enhanced surface expression of intercellular adhesion molecule, vascular cell adhesion molecule, and E-selectin.
Results suggest that beta 2-GPI deposition on either resting or activated endothelial cells and modulation of its proposed in vivo anticoagulant activity through subsequent aCL antibody binding does not account for the thrombotic manifestations of APS.
检测β2-糖蛋白I（β2-GPI）的结合情况及其在体外增强IgG抗心磷脂（aCL）抗体与静息及细胞因子激活的内皮细胞结合的能力。评估IgG aCL抗体阳性血清在体外诱导内皮细胞激活的能力。
通过亲和纯化从6例系统性红斑狼疮（SLE）患者和3例原发性抗磷脂抗体综合征（APS）患者中分离出具有aCL活性的IgG。人脐静脉内皮细胞（HUVEC）在无血清条件下培养，并在静息状态或用肿瘤坏死因子α（TNF-α）激活后进行检测。HUVEC分别暴露于单独的β2-GPI、单独的IgG或IgG加β2-GPI。最后，我们检测了来自相同SLE和原发性APS患者的血清在培养中激活HUVEC的能力。
β2-GPI、IgG aCL或IgG aCL加β2-GPI均未与静息或细胞因子激活的内皮细胞结合。此外，通过细胞间黏附分子、血管细胞黏附分子和E-选择素的表面表达增强评估，相同患者的血清未在体外诱导内皮细胞激活。
结果表明，β2-GPI在静息或激活的内皮细胞上的沉积以及通过随后的aCL抗体结合对其体内抗凝活性的调节并不能解释APS的血栓形成表现。
