Thrombogenic properties of antiphospholipid antibodies do not depend on their binding to beta2 glycoprotein 1 (beta2GP1) alone.

Abstract

Immunization of mice with beta2glycoprotein 1 (beta2GP1) induces production of antiphospholipid (aPL) antibodies, which were shown to have thrombus enhancing properties in an experimental mouse model, indicating that these antibodies are thrombogenic in vivo. To determine whether the thrombogenic effect of murine antiphospholipid antibodies is due to their aPL or their anti-beta2GP1 activity, we injected mice with murine monoclonal anticardiolipin (aCL) and anti-beta2GP1 antibodies. Effects of these antibodies on thrombus formation, was evaluated utilizing a mouse model which enables kinetics of thrombus formation to be studied. The results of this study showed that the size of the thrombus in animals injected with murine aCL antibodies was larger than that in control groups. There was no difference in thrombus kinetics between anti-beta2GP1 injected mice and controls, suggesting that the thrombogenic effect of aPL antibodies is not related to their anti-beta2GP1 activity alone. Mice receiving monoclonal antibodies with both aCL and anti-beta2GP1 activity, also increase thrombus size when compared with controls. These data indicate that murine aCL, but not anti-beta2GP1, antibodies are thrombogenic in vivo.