Role of β2-glycoprotein I in the pathogenesis of the antiphospholipid syndrome  

作　　者：Jing Li Xiangrui Zhu Juan Feng 

机构地区：[1]Department of Endocrinology,Beijing ChaoYang Hospital,Capital Medical University,Beijing,China [2]Department of Physiology and Pathophysiology,School of Basic Medical Sciences,Peking University,Beijing,China [3]Department of Integration of Chinese and Western Medicine,School of Basic Medical Sciences,Peking University,Beijing,China

出　　处：《Rheumatology & Autoimmunity》2023年第3期131-139,共9页风湿病与自身免疫（英文）

基　　金：National Natural Science Foundation of China,Grant/Award Numbers:92268107,82170476;Natural Science Foundation of Beijing,China,Grant/Award Number:M21008。

摘　　要：Antiphospholipid syndrome(APS)is typically characterized by increased levels of three classes of antiphospholipid antibodies,namely lupus anticoagulant,anti-β2-glycoprotein I(anti-β2GPI),and anticardiolipin antibodies.β2-Glycoprotein(β2GPI)is a phospholipid-binding protein composed of five domains(DI-V)and a major antigen in APS.β2GPI is expressed on the surfaces of several cell types,including endothelial cells,monocytes,trophoblast cells,and platelets.Its binding to the anti-β2GPI antibody triggers downstream signaling events and ultimately exerts a variety of cellular effects.β2GPI modulates hemostasis and the complement system,as well as playing an important role in APS-associated vascular injury.Therefore,studying β2GPI will help elucidate the pathogenesis of APS and improve the treatment of patients with this condition.This review will mainly focus on the structure and function of β2GPI,as well as its implication in the pathogenesis of APS.

关 键 词：antiphospholipid syndrome COAGULATION COMPLEMENT INFLAMMATION β2-glycoprotein I 

分 类 号：R73[医药卫生—肿瘤]