Anticardiolipin antibodies in NZW x BXSB F1 mice: A model of antiphospholipid syndrome

Y. Hashimoto, M. Kawamura, K. Ichikawa, T. Suzuki, T. Sumida, S. Yoshida, E. Matsuura, S. Ikehara, T. Koike

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Abstract

NZW x BXSB F1 (W/B F1) male mice develop systemic lupus-like disease, and several autoantibodies, circulating immune complexes, and lupus nephritis become apparent. The abnormally high incidence of degenerative coronary vascular disease with myocardial infarction and thrombocytopenia due to the presence of both platelet-associated antibodies and circulating antiplatelet antibodies in this animal has been reported. We found that W/B F1 male mice produced autoantibodies against cardiolipin (aCL) and that the titer of aCL increases with age. aCL from W/B F1 male mice were mainly IgG and binding activity to cardiolipin was aCL-cofactor (β2-glycoprotein I (β2-GPI)) dependent. We developed monoclonal aCL from these animals and examined specificity of the autoantibodies. All the mAb used reacted with the negatively charged phospholipids, cardiolipin, phosphatidylserine, and phosphatidylinositol, and some reacted with platelets and DNA. The addition of human or mouse β2-GPI enhanced the titer for monoclonal aCL from the W/B F1 mice. From the results of competitive inhibition enzyme immunoassay with monoclonal aCL and purified β2-GPI, aCL from the W/B F1 mice recognized the complex of CL and β2-GPI. The W/B F1 male mouse may be an appropriate model for use in studies on the pathologic significance of aCL in patients with antiphospholipid syndrome.

Original languageEnglish
Pages (from-to)1063-1068
Number of pages6
JournalJournal of Immunology
Volume149
Issue number3
Publication statusPublished - Jan 1 1992
Externally publishedYes

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ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

Cite this

Hashimoto, Y., Kawamura, M., Ichikawa, K., Suzuki, T., Sumida, T., Yoshida, S., Matsuura, E., Ikehara, S., & Koike, T. (1992). Anticardiolipin antibodies in NZW x BXSB F1 mice: A model of antiphospholipid syndrome. Journal of Immunology, 149(3), 1063-1068.