Immunization of naive BALB/c mice with human β2-glycoprotein I breaks tolerance to the murine molecule

A. Tincani, B. Gilburd, M. Abu-Shakra, M. Blank, F. Allegri, R. Ottaviani, M. Riboni, P. L. Meroni, G. Balestrieri, Y. Shoenfeld*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


Objective. Immunization of naive mice with β2 glycoprotein I (β2GPI) leads to the generation of pathogenic anticardiolipin antibodies associated with clinical manifestations of the antiphospholipid syndrome (APS). The aim of this study was to determine whether immunization of naive mice with human β2GPI, which shares homology with mouse β2GPI molecules, breaks tolerance to murine β2GPI and leads to the generation of anti-mouse β2GPI. Methods. Twenty-four female BALB/c mice were immunized in the footpads with 10 μg of human β2GPI. Twelve age- and sex-matched BALB/c mice were immunized in the same manner with Freund's complete adjuvant and served as controls. The reactivity of whole sera, polyclonal IgG, and affinity-purified anti-β2GPI IgG antibodies against human, bovine, and mouse β2GPI was evaluated by enzyme-linked immunosorbent assay. Results. High titers of anti-human β2GPI IgG antibodies were detected I month after immunization. Progressively increasing titers against murine and bovine β2GPI were recorded 1-4 months after injection. Conclusion. Immunization of mice with human β2GPI resulted in the generation of antibodies reacting with human, bovine, and murine β2GPI. The loss of tolerance to mouse β2GPI is attributable to the high interspecies homology of β2GPI. These results may point to molecular mimicry as a possible cause of APS.

Original languageEnglish
Pages (from-to)1399-1404
Number of pages6
JournalArthritis and Rheumatism
Issue number5
StatePublished - 2002


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