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This article is part of the supplement: 23rd European Workshop for Rheumatology Research

Meeting abstract

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

M Blank, I Krause1, M Fridkin2, N Keller1, J Kopolovic1, I Goldberg1, A Tobar1 and Y Shoenfeld1

Author Affiliations

1 Center for of Autoimmune Diseases, Department of Internal Medicine 'B', The Weizmann Institute of Science, Rehovot, Israel

2 Department of Organic Chemistry, The Weizmann Institute of Science, Rehovot, Israel

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Arthritis Res Ther 2003, 5(Suppl 1):14  doi:10.1186/ar644


The electronic version of this article is the complete one and can be found online at:


Published:24 February 2003

©

Meeting abstract

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.