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Publication Detail
In vivo inhibition of antiphospholipid antibody-induced pathogenicity utilizing the antigenic target peptide domain I of beta-glycoprotein I: proof of concept
  • Publication Type:
    Journal article
  • Publication Sub Type:
  • Authors:
    Ioannou Y, Romay-Penabad Z, Pericleous C, Giles I, Papalardo E, Vargas G, Shilagard T, Latchman DS, Isenberg DA, Rahman A, Pierangeli S
  • Publication date:
  • Pagination:
    833, 842
  • Journal:
    Journal of Thrombosis and Haemostasis
  • Volume:
  • Issue:
  • Print ISSN:
  • Keywords:
    analysis, Antibodies, Cell Adhesion, development, Macrophages, methods, Mice, Mutation, pathogenicity, Research, Rheumatology, Syndrome, Vascular Cell Adhesion Molecule-1
  • Addresses:
    Centre for Rheumatology Research, Windeyer Building, University College London, London, UK
Summary Objectives: In the antiphospholipid syndrome (APS) the immunodominant epitope for the majority of circulating pathogenic antiphospholipid antibodies (aPL) is the N-terminal domain (DI) of ss(2)glycoprotein I (ss(2)GPI). We have previously shown that recombinant DI inhibits aPL in fluid-phase from binding to immobilized native antigen and this inhibition was enhanced with the mutant DI(D8S,D9G)and lost with the DI(R39S) mutation. Hence we hypothesized that DI and the DI(D8S,D9G) mutant would inhibit aPL-induced pathogenicity in vivo. Methods: C57BL/6 mice (n=5, each group) were injected with APS purified IgG (IgG-APS, 500mug) or IgG from healthy volunteers (IgG-NHS) and either recombinant DI, the mutants DI(R39S) or DI(D8S,D9G) or an irrelevant control peptide (at 10-40mug). Outcome variables measured were analysis of femoral vein thrombus dynamics in treated and control groups following standardized vessel injury, expression of vascular cell adhesion molecule-1 (VCAM-1) on the aortic endothelial surface and tissue factor (TF) activity in murine macrophages. Results: IgG-APS significantly increased thrombus size compared with IgG-NHS. The IgG-APS thrombus enhancement effect was abolished in mice pre-treated with recombinant DI (p
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