Antiphospholipid Syndrome by A. Bulikova

By A. Bulikova

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Extra resources for Antiphospholipid Syndrome

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1999. Beta2-glycoprotein I is proteolytically cleaved in vivo upon activation of fibrinolysis. Thromb Haemost 81:87-95. A. 2008. Beta2-glycoprotein I protects thrombin from inhibition by heparin cofactor II: potentiation of this effect in the presence of anti-beta2-glycoprotein I autoantibodies. Arthritis Rheum 58:1146-1155. , and Suzuki, K. 1996. beta 2Glycoprotein I modulates the anticoagulant activity of activated protein C on the phospholipid surface. Thromb Haemost 75:49-55. A. 2001. Impaired thrombin generation in beta 2-glycoprotein I null mice.

For many years the characterization of the antibodies was the line of approach to understand the pathophysiology of the syndrome, unfortunately with little success. During the last years, more and more evidence has become available that β2GPI is a more general scavenger in our circulation. Maiti et al (2008) showed a β2GPI-dependent phosphatidylserine (PS) expressing apoptotic cell uptake by macrophages. Binding of β2GPI to these cells caused recognition and uptake of the β2GPI-apoptotic cell complex by the LRP receptor on macrophages.

In press. Arad A, Proulle V, Furie RA, Furie BC & Furie B. (2011) β₂-Glycoprotein-1 autoantibodies from patients with antiphospholipid syndrome are sufficient to potentiate arterial thrombus formation in a mouse model. Blood. 117(12), 3453-3459. Bevers EM & Galli M. (1990) Beta 2-glycoprotein I for binding of anticardiolipin antibodies to cardiolipin. Lancet. 336(8720), 952-953. Birdsall MA, Pattison NS & Chamley LW. (1992) Antiphospholipid antibodies in pregnancy. J Obstet Gynaecol. 32, 328-330.

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