A potential anti-coagulant role of complement factor H

Abstract

Anti-phospholipid syndrome (APS) is a complex autoimmune disease, associated with recurrent venous and arterial thrombosis in various tissues. APS is associated with specific antibodies against plasma beta-2 glycoprotein 1 (β2-GP1), and these antibodies react with β2-GP1 bound to negatively charged phospholipids (e.g. cardiolipin) on cell membranes. Some APS patients also have autoantibodies to complement factor H (FH), a homologue of β2-GP1, which also binds to anionic phospholipids. β2-GP1 has earlier been shown to inhibit the intrinsic (contact) activated blood coagulation pathway, promoted by anionic phospholipids. Here we examine whether FH could have similar anti-thrombotic properties. In vitro experiments with surface-bound phospholipids and human plasma, in the presence of FH, confirm this hitherto unreported property of FH.