Anti-endothelial cell antibody and thrombosis

1.血管内皮细胞(EC)表面存在一种类似肝素的五糖结构，称为血管五糖(VPS)，通过与抗凝血酶III(ATIII)结合发挥抗凝作用。建立了一种简便、灵敏的检测血清抗VPS抗体的酶联免疫吸附试验。86例血栓形成患者中18例(20.9%)检出抗VPS抗体，34例反复流产患者中14例(46.7%)检出抗VPS抗体，3例(2.7%)无血栓病史的III患者中检出抗VPS抗体。32例抗VPS阳性患者中，12例诊断为抗磷脂抗体综合征(APS)。18例抗VPS阳性血栓形成患者中8例和14例抗VPS阳性反复流产患者中12例抗磷脂抗体(APL)阴性，包括抗心磷脂抗体、狼疮抗凝剂或Anri-凝血酶原抗体。我们研制了产生抗VPS抗体的杂交瘤细胞。血清和人源性抗VPS单抗对VPS和EC均有较好的特异性，而对心磷脂、β2-糖蛋白和DNA3种抗体均无明显的特异性。给妊娠小鼠注射ARE抗VPS单抗不能引起自然流产，但可引起小鼠凝血酶-抗凝血酶水平升高。这些结果向APS表明。结论：1.检测抗VPS抗体有助于自身免疫性血栓形成或流产的诊断。(1)血清和抗VPS单抗均能与人脐血管内皮细胞(HUVEC)结合，导致CD62P表达，增强HUVEC与T细胞的结合。

1. A heparin-like pentasaccharide structure, termed vascular pentasaccharide (VPS), on the surface of endothelial cells(EC) contributes to anticoagulation in the circulation through the binding to antithrombin III(ATIII). We developed a simple and sensitive ELISA to detect anti-VPS antibodies in sera. Anti-VPS antibodies were detected in 18(20.9%) of 86patients with thrombisis, 14(46.7%) of 34 with recurrent abortion, and 3(2.7%) of III with no history of thrombotic of episodes. Among 32 anti-VPS positive patients, 12 were diagnosed antihospholopid antibody syndrome(APS). Eight of 18 anti-VPS-positive patients with thrombosis, and 12 of 14 anti-VPS-positive patients with recurrent abortin showed negative tests for anti-phospholipid antibody(aPL) including anti-cardiolipin antibody, lupus anticoagulant or anri-prothrombin antibody. We developed were hybridoma producing anti-VPS antibody. Both serum and human monoclonal anti-VPS antbodies showed a fine specificity to VPS (ATIII binding site) and EC, but not to cardioripin, β2-glycoprotein or DNA. Administration of were monoclonal anti VPS antibody to pregnant mice failed to cause spontaneous abortion, but, caused the elevation of thrombin-antithtombin levels in the mice. These results indicate to APS. The detection of anti-VPS antibodies can contribute to the diagnosis of autoimmune thrombosis or abortion.2. (1)Serum and monoclonal anti VPS antibodies had an ability to bind human umbilical vascular endothelial cells(HUVEC), resulting in causing, the expression of CD62P and enhancing HUVEC binding of T cells.