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.
Titolo: | BINDING OF AUTOIMMUNE CARDIOLIPIN-REACTIVE ANTIBODIES TO HEPARIN - A MECHANISM OF THROMBOSIS | |
Autori: | ||
Data di pubblicazione: | 1995 | |
Rivista: | ||
Abstract: | 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. | |
Handle: | http://hdl.handle.net/11577/132179 | |
Appare nelle tipologie: | 01.01 - Articolo in rivista |