Abstract
Antiphospholipid syndrome (APS) is characterized by arterial and/or venous thrombosis and pregnancy morbidity in the presence of antiphospholipid antibodies (aPL). β2-glycoprotein I(β2-GPI) and prothrombin are representative autoantigens, the former more extensively investigated. Anti-β2-GPI antibodies are not only markers of APS, but also are considered to be pathogenic. Possible roles of anti-β2-GPI antibodies are, 1) enhancement the binding of β2-GPI to anionic phospholipid and inhibition of protein C activation/activated protein C, 2) to form anti-β2-GPI antibody-β2-GPI-oxidized LDL complex and to promote uptake by sub-endothelial macrophage, resulting in atherosclerosis, 3) to dimerize β2-GPI on the surface of platelets and to activate platelets via apoE receptor 2 and subsequent signal transduction, 4) stimulation of monocytes via p38 MAP kinase pathway and induction of tissue factor production. In pregnancy morbidity, activation of complement cascade plays an important role. These findings may provide a novel target in the management of APS.
