Thromb Haemost 2001; 85(01): 57-62
DOI: 10.1055/s-0037-1612904
Review Article
Schattauer GmbH

Some Patients with Antiphospholipid Syndrome Express hitherto Undescribed Antibodies to Cardiolipin-binding Proteins

P. Rampazzo
1   Department of Clinical and Experimental Medicine, Thrombosis Center, University of Padova, Italy
,
A. Biasiolo
1   Department of Clinical and Experimental Medicine, Thrombosis Center, University of Padova, Italy
,
J. Garin
1   CEA/Grenoble Laboratoire de Chimie des Proteines, Grenoble Cedex, France
,
A. Rosato
2   Dept. of Oncology and Surgical Sciences, University of Padova, Italy
,
C. Betterle
3   Dept. of Medical and Surgical Sciences, University of Padova, Italy
,
A. Ruffatti
3   Dept. of Medical and Surgical Sciences, University of Padova, Italy
,
V. Pengo
1   Department of Clinical and Experimental Medicine, Thrombosis Center, University of Padova, Italy
› Institutsangaben
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Publikationsverlauf

Received 22. Dezember 1999

Accepted after resubmission 06. September 2000

Publikationsdatum:
08. Dezember 2017 (online)

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Summary

Contrary to infective anticardiolipin (aCL) antibodies, autoimmune aCL antibodies react with phospholipids (PL) mainly via binding to the plasma glycoprotein cofactor β2-Glycoprotein I (β2GPI). While there is a well-documented link between the risk of thrombosis and the presence of β2GPI-dependent anticardiolipin antibodies, the pathological impact of other antiphospholipid antibodies is less clear. By means of cardiolipin affinity-chromatography, we isolated and identified 3 CL-binding proteins, complement component C4, complement factor H and a kallikrein-sensitive glycoprotein, and tested for the presence of autoantibodies against these proteins in patients with antiphospholipid syndrome (APS), systemic lupus erythematosus (SLE) and other autoimmune diseases. High titers of autoantibodies to C4 as compared to age- and sex-matched healthy controls were present in 3 of 26 patients with APS, and weak titers were found in 2 of 26 patients with SLE and in none of 26 patients with other autoimmune diseases. Autoantibodies to complement factor H were found in 4 APS, 3 SLE and none of the other autoimmune patients. Autoantibodies to kallikrein-sensitive glycoprotein were detected in 6 APS patients, 1 SLE patient, and 1 patient with another autoimmune disease. A close relationship between these antibodies was found, suggesting their origin from a common macromolecular complex. However, no relationship with anti-β2GPI antibodies was found, with the three patients with higher levels of autoantibodies having a low titer of anti-β2GPI antibodies. In conclusion, some patients with APS harbor circulating antibodies to other CL-binding proteins which might be useful to further characterize these patients.