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Publication Detail
beta 2 glycoprotein-I inhibits factor XII activation on triglyceride rich lipoproteins: the effect of antibodies from plasma of patients with antiphospholipid syndrome.
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    McNally T, Mackie IJ, Isenberg DA, Machin SJ
  • Publication date:
    08/1996
  • Pagination:
    220, 225
  • Journal:
    Thromb Haemost
  • Volume:
    76
  • Issue:
    2
  • Status:
    Published
  • Country:
    Germany
  • Print ISSN:
    0340-6245
  • Language:
    eng
  • Keywords:
    Adult, Antibodies, Antibodies, Anticardiolipin, Antiphospholipid Syndrome, Case-Control Studies, Factor XIIa, Female, Glycoproteins, Humans, Immunoglobulin G, Lipoproteins, VLDL, Male, Middle Aged, Triglycerides, beta 2-Glycoprotein I
Abstract
It is now well recognised that antiphospholipid antibodies are associated with thrombosis and recurrent fetal loss. Some antiphospholipid antibodies (aPAs) have been shown to require a cofactor, beta 2 glycoprotein-I (beta 2 GPI), for binding to phospholipids, and recently beta 2 GPI has been identified as the antigenic target for some aPAs. beta 2 GPI possesses in vitro anticoagulant properties and modulation of beta 2 GPI function may therefore result in altered haemostatic regulation. In the present study, the influence of plasma derived aPAs and beta 2 GPI on factor XII activation on the surface of very low density lipoprotein (VLDL) was investigated. Factor XIIa generation was dependent on lipoprotein lipase treatment of VLDL and beta 2 GPI inhibited the factor XIIa generation in a concentration dependent manner. No consistent effects on factor XIIa generation were demonstrated with the IgG fractions from patients with aPAs. Inhibition of the beta 2 GPI activity was demonstrated by some antibodies, and study with cardiolipin affinity purified antibody indicated that antibody concentration is critical. These results suggest that perturbation of beta 2 GPI function may contribute to the pathogenic mechanism for thrombosis in some patients with aPAs.
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