Requirement of activation of complement C3 and C5 for antiphospholipid antibody-mediated thrombophilia.

摘要: Objective Antiphospholipid antibodies (aPL) have been shown to induce thrombosis, activate endothelial cells, and fetal loss. The pathogenesis of aPL-induced although not completely understood, may involve platelet cell activation as well procoagulant effects aPL directly on clotting pathway components. Recent studies that uncontrolled complement leads death in aPL-treated mice. In this study, we tested the hypothesis are responsible for complement, thus generating split products thrombosis. Methods To study thrombus dynamics adhesion leukocytes used vivo murine models thrombosis microcirculation, which injections were used. Results Mice deficient components C3 C5 resistant enhanced was induced by aPL. Furthermore, inhibition using anti-C5 monoclonal prevented thrombophilia aPL. Conclusion These data show mediates 2 important effectors aPL, induction cells.