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抗磷脂综合征的体内血栓形成模型。

In vivo models of thrombosis for the antiphospholipid syndrome.

作者信息

Pierangeli S S, Harris E N

机构信息

Department of Microbiology and Immunology, Morehouse School of Medicine, Atlanta, GA 30310-1495, USA.

出版信息

Lupus. 1996 Oct;5(5):451-5. doi: 10.1177/096120339600500524.

DOI:10.1177/096120339600500524
PMID:8902780
Abstract

Utilizing this unique animal model of thrombosis we demonstrated that human (IgG, IgM or IgA) polyclonal and monoclonal antiphospholipid antibodies derived from APS patients have a significant enhancing effect on thrombus formation. This effect is reversed by treatment of the mice with hydroxychloroquine (plaquenil). In addition murine polyclonal and monoclonal anticardiolipin antibodies induced by active immunization with human beta 2-GP1 or human anticardiolipin antibodies showed to have thrombogenic properties in CD1 mice. Antibodies with antihuman beta 2-GP1 activity alone did not seem to affect thrombus formation.

摘要

利用这种独特的血栓形成动物模型,我们证明,源自抗磷脂综合征(APS)患者的人源(IgG、IgM或IgA)多克隆和单克隆抗磷脂抗体对血栓形成具有显著的增强作用。用羟氯喹(氯喹)治疗小鼠可逆转这种作用。此外,用人类β2 -糖蛋白1或人类抗心磷脂抗体进行主动免疫诱导的鼠源多克隆和单克隆抗心磷脂抗体在CD1小鼠中显示出具有血栓形成特性。单独具有抗人类β2 -糖蛋白1活性的抗体似乎不会影响血栓形成。

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In vivo models of thrombosis for the antiphospholipid syndrome.抗磷脂综合征的体内血栓形成模型。
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Thrombogenic properties of antiphospholipid antibodies do not depend on their binding to beta2 glycoprotein 1 (beta2GP1) alone.抗磷脂抗体的血栓形成特性并不仅取决于它们与β2糖蛋白1(β2GP1)的结合。
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