Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Kita-ku, Okayama, Japan.
Lupus. 2010 Apr;19(4):379-84. doi: 10.1177/0961203310361352.
Since beta(2)-glycoprotein I (beta(2)GPI) was described as the major antigenic target for antiphospholipid antibodies, many studies have focused their attention to the physiological role of beta(2)GPI and anti-beta(2)GPI antibodies on autoimmune-mediated thrombosis. Studies reporting the physiological role of beta(2)GPI have been numerous, but the exact mechanism of action(s) has yet to be completely determined. beta(2)GPI's epitopes for anti-beta(2)GPI autoantibodies have been characterized, however, not all of the heterogeneous anti-beta(2)GPI antibodies are pathogenic. The pathophysiologic role of beta(2)GPI has been reported in the fields of coagulation, fibrinolysis, angiogenesis, and atherosclerosis. Our understanding of the impact of beta(2)GPI, its metabolites and autoantibodies to beta(2)GPI on these physiological functions may contribute to the development of better therapeutic strategies to treat and prevent autoimmune-mediated atherothrombotic vascular disease.
自从β2-糖蛋白 I(β2GPI)被描述为抗磷脂抗体的主要抗原靶标以来,许多研究都集中在β2GPI 和抗β2GPI 抗体在自身免疫性介导的血栓形成中的生理作用上。关于β2GPI 的生理作用的研究报告很多,但确切的作用机制尚未完全确定。β2GPI 的抗β2GPI 自身抗体表位已经得到了描述,然而,并非所有的异质性抗β2GPI 抗体都是致病性的。β2GPI 在凝血、纤溶、血管生成和动脉粥样硬化等领域的病理生理作用已经有报道。我们对β2GPI、其代谢物和抗β2GPI 自身抗体对这些生理功能的影响的理解可能有助于开发更好的治疗策略,以治疗和预防自身免疫性动脉粥样硬化性血管疾病。