ANTI-BETA(2)-GLYCOPROTEIN-I ANTIBODIES AND THROMBOSIS

Taken together, these results clarify the relationships between ACA and LA, but no simple explanation for thrombosis can be drawn from them. An effect of anti-β2-GPI antibodies on platelet activation would be a first indication, but interactions with endothelial cells, although not described until now (38), are not excluded, since previous results indicated interactions between APLA and the endothelium (39, 40). One must consider the possibility that β2-GPI interactions with phospholipids may lead to conformational changes and heterogeneous recognition by the different populations of autoantibodies involved in this setting (ACA and LA, corresponding to reactivity with various lipid-protein complexes). However, direct in vivo evidence that immunization with β2-GPI or passive transfer of anti-β2-GPI antibodies in laboratory animals can induce APLS features would be a clear confirmation of the probable central part played by β2-GPI in these phenomena. © 1995 Humana Press Inc.