Arthritis Res Ther

, 5:14 | Cite as

The infectious origin of the antiphospholipid syndrome: induction by passive transfer of anti-β2GPI antibodies induced by common bacteria

  • M Blank
  • I Krause
  • M Fridkin
  • N Keller
  • J Kopolovic
  • I Goldberg
  • A Tobar
  • Y Shoenfeld
Meeting abstract
  • 1.7k Downloads

Keywords

Tetanus Haemophilus Influenzae Tetanus Toxoid Fetal Loss Immunize Mouse 

The antiphospholipid syndrome (APS) is characterized by the presence of pathogenic autoantibodies against β2-glycoprotein I (β2GPI). The factors causing production of anti-β2GPI remain unidentified, but an association with infectious agents has been reported. We recently identified a hexapeptide (TLRVYK) that is recognized specifically by a pathogenic anti-β2GPI monoclonal antibody. In the present study we evaluated the APS-related pathogenic potential of microbial pathogens, which share structural homology with the this hexapeptide. Mice were immunized with a panel of TLRVYK-related microbial particles and were studied for the development of mouse anti-β2GPI autoantibodies. Mouse IgG specific to the TLRVYK peptide were affinity purified from the immunized mice and passively infused i.v. into naive mice at day 0 of pregnancy. APS parameters were evaluated in the infused mice on day 15 of pregnancy. Following immunization, high titers of anti-peptide, anti-β2GPI antibodies were observed in mice immunized with Haemophilus influenzae, Neisseria gonorrhoeae or tetanus toxoid. Naive mice infused with the affinity-purified anti-peptide antibodies had a significant thrombocytopenia, prolonged aPTT and elevated percentage of fetal loss, similar to the findings in a control group of mice immunized with a pathogenic anti-β2GPI monoclonal antibody. Our study establishes a mechanism of molecular mimicry in experimental APS, demonstrating that bacteria homologous with β2GPI structure are able to induce the generation of pathogenic anti-β2GPI antibodies along with APS manifestations.

Copyright information

© The Author(s) 2003

Authors and Affiliations

  • M Blank
  • I Krause
    • 1
  • M Fridkin
    • 2
  • N Keller
    • 1
  • J Kopolovic
    • 1
  • I Goldberg
    • 1
  • A Tobar
    • 1
  • Y Shoenfeld
    • 1
  1. 1.Center for of Autoimmune Diseases, Department of Internal Medicine 'B'The Weizmann Institute of ScienceRehovotIsrael
  2. 2.Department of Organic ChemistryThe Weizmann Institute of ScienceRehovotIsrael

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