Pathophysiology of beta2-glycoprotein I in antiphospholipid syndrome

• Published in: Lupus 2010-04, Vol.19 (4), p.379-384
• Main Authors: Matsuura, E, Shen, L, Matsunami, Y, Quan, N, Makarova, M, Geske, F J, Boisen, M, Yasuda, S, Kobayashi, K, Lopez, L R
• Format: Article
• Language: English
• Subjects: Animals; Antiphospholipid Syndrome - complications; Antiphospholipid Syndrome - immunology; Antiphospholipid Syndrome - physiopathology; Atherosclerosis - etiology; Atherosclerosis - physiopathology; Autoantibodies - immunology; beta 2-Glycoprotein I - immunology; Blood Coagulation - physiology; Epitopes; Humans; Neovascularization, Pathologic - physiopathology; Thrombosis - etiology; Thrombosis - physiopathology
• ISSN: 1477-0962
• 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.