Binding of autoimmune cardiolipin-reactive antibodies to heparin: a mechanism of thrombosis?
Autoimmune CL-rA need a plasma protein, beta 2GPI, to bind anionic PL. While beta 2GPI could be the true antigen, beta 2GPI binding to solid phase heparin did not determine its recognition by CL-rA when using patient plasmas. We tested plasmas from four patients with antiphospholipid syndrome in this study and no CL-rA binding to heparin sepharose was obtained. On the contrary, when CL-rA were first purified from the plasmas by means of a CL-octyl sepharose column, the purified material bound to the heparin sepharose column. Thus, after recognizing beta 2 GPI, CL-rA bind heparin. 'In vivo' CL-rA binding to heparin like-substances could inhibit the anti-thrombotic properties of endothelial cells.
Pengo
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V
Dept. of Cardiology, University of Padua School of Medicine, Italy.
Biasiolo
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A
Fior
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MG
D000328:Adult; D017153:Antibodies, Anticardiolipin / Q000302:isolation & purification / Q000378:metabolism*; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000276:immunology; D002846:Chromatography, Affinity; D005260:Female; D006023:Glycoproteins / Q000276:immunology / Q000378:metabolism; D006493:Heparin / Q000378:metabolism*; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000378:metabolism; D008297:Male; D011485:Protein Binding; D013927:Thrombosis / Q000209:etiology*; D053482:beta 2-Glycoprotein I
D017153:Antibodies, Anticardiolipin; D006023:Glycoproteins; D016682:Lupus Coagulation Inhibitor; D053482:beta 2-Glycoprotein I; D006493:Heparin