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 Blood, 1 October 2005, Vol. 106, No. 7, pp. 2340-2346.
Prepublished online as a Blood First Edition Paper on June 14, 2005; DOI 10.1182/blood-2005-03-1319.

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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY

Thrombus formation induced by antibodies to {beta}2-glycoprotein I is complement dependent and requires a priming factor

Fabio Fischetti, Paolo Durigutto, Valentina Pellis, Alessandra Debeus, Paolo Macor, Roberta Bulla, Fleur Bossi, Federica Ziller, Daniele Sblattero, Pierluigi Meroni, and Francesco Tedesco

From the Department of Physiology and Pathology, University of Trieste, Trieste, Italy; the Department of Medicine and Neurology, University of Trieste, Trieste, Italy; the Department of Medical Sciences, University of Eastern Piedmont, Vercelli, Italy; and the Department of Internal Medicine, Allergy and Clinical Immunology Section, IRCCS Istituto Auxologico Italiano, University of Milan, Milan, Italy.

We monitored the number of intravascular platelet-leukocyte aggregates (PLAs) and thrombotic occlusions (TOs) by intravascular microscopy in the mesentery of rats receiving antiphospholipid (aPL) immunoglobulin G (IgG) purified from the sera of patients with antiphospholipid syndrome. aPL IgG had no procoagulant effect, but it caused rapid endothelial deposition of fibrinogen, followed by PLA and TO in rats receiving an intraperitoneal injection of bacterial lipopolysaccharide 3 hours before IgG infusion. Anti-{beta}2-glycoprotein I-depleted aPL IgG failed to induce PLAs and TOs. C3 and C9 colocalized with aPL IgG on the mesenteric vessels. The number of PLAs and TOs was markedly reduced in C6-deficient rats and in animals treated with anti-C5 miniantibody, suggesting the contribution of the terminal complement (C) complex to the aPL antibody-mediated intravascular thrombosis. In conclusion, our data indicate that antibodies to {beta}2-glycoprotein I trigger coagulation subsequent to a priming proinflammatory factor and that the terminal C complex is the main mediator of the coagulation process.


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