It has been reported that antiphospholipid autoantibodies do not recognize phospholipid alone, but rather the plasma protein j2-glycoprotein I (,B2GPI), or a ,B2GPI-phospholipid complex. In vitro #2GPI binds to anionic phospholipids and inhibits the prothrombinase activity of procoagulant membranes. In light of the fact that lupus anticoagulants, a type of antiphospholipid antibody, have similar anticoagulant properties, the relationship of ,B2GPI to lupus anticoagulant activity was investigated. IgG from patients with autoimmune diseases or syphilis were tested for anticardiolipin reactivity and lupus anticoagulant activity in the presence and absence of #2GPI. As expected, anticardiolipin reactivity associated with autoimmune disease was ,B2GPI dependent. In contrast, IgG from a patient with syphilis recognized cardiolipin alone and binding was inhibited by ,B2GPI. Autoimmune antiphospholipid antibodies prolonged the dilute Russell viper venom time of normal plasma, but had no effect onf2GPI-depleted plasma. Antiphospholipid antibodies associated with syphilis had no anticoagulant effect. RP-1, an anti-,B2GPI mAb, had anticoagulant effects similar to those ofautoimmune antiphospholipid antibodies. These data demonstrate that antiphospholipid autoantibodies exert lupus anticoagulant activity via an interaction with ,82GPI. These antibodies and RP-1 appear to amplify the anticoagulant effect of ,B2GPI itself. (J. Clin. Invest. 1992. 90:1100-1104

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