Summary

The antiphospholipid syndrome (APS) refers to persistent anti-phospholipidantibodies (aPL) associated with thromboticand/or obstetrical complications. The endothelial cell is a targetof aPL which can induce a procoagulant and proinflammatoryendothelial phenotype, as reported both in vivo and in vitro.Microparticle production is a hallmark of cell activation. In thepresent study, the presence of endothelial microparticles (EMP)in the plasma of APS patients was investigated. To determineif there is a correlation with certain biological and clinicalfeatures, EMP levels were measured in thrombosis-free patientswith systemic lupus erythematosus (SLE) patients, with andwithout aPL, in patients with non aPL-related thrombosis, aswell as in healthy controls. Compared to healthy subjects,elevated plasma levels of EMP were found in patients with APS and in SLE patients with aPL, but not in SLE patients withoutaPL or in non aPL-related thrombosis. EMP levels were alsoassociated with Lupus Anticoagulant (LA) detected by a positiveDilute Russell’s Viper Venom time (DRVVT). In parallel, weanalyzed the capacity of these plasma to induce vesiculation ofcultured endothelial cells. We demonstrated an increase ofEMP generated in response to plasma from patients with autoimmunediseases. Interestingly, only APS plasma induced therelease of EMP with procoagulant activity. These ex vivo and invitro observations indicate that generation of EMP in APS andSLE patients results from an autoimmune process involving aPL.Production of procoagulant microparticles in APS patients mayrepresent a new pathogenic mechanism for the thromboticcomplications of this disease.