Anti-beta2-glycoprotein I antibodies and anti-endothelial cell antibodies induce tissue factor in endothelial cells

Anti-beta2-glycoprotein I antibodies bind to endothelial cells through beta 2-GPI. The antibodies are present in patients with systemic lupus erythemat osus and antiphospholipid syndrome and are associated with the pathogenesis of the disease. Anti-endothelial cell antibodies that react with constitut ive antigens on ECs are present in patients with vasculiditis and other dis eases. Both types of antibodies can activate ECs. Frequent findings in APLS and vasculitis are fibrin deposits and thromboembolic phenomena. These ind icate that the coagulation system is activated. However, the mechanism of a ctivation is not clear. ECs generate tissue factor upon stimulation with va rious substances. In the present study we report that monoclonal anti-beta2 -GPI antibodies and AECAs, derived from a patient with primary APLS and a p atient with Takayasu's arteritis, respectively, induce a potent tissue fact or in ECs. The production of TF activity, TF antigen and TF mRNA is dose an d time dependent. The TF activity was induced also by F(ab)(2) but not by F c fragments and was abolished completely by pre-incubation with ant-TF anti bodies. The TF that is induced in ECs by AECAs with and without beta2-GPI s pecificity may activate the coagulation and thereby play a major role in th e pathogenesis of fibrin deposition and thrombus formation in diseases that are associated with the presence of these antibodies.