Monoclonal anticardiolipin autoantibodies established from the (new zealand white x bxsb)f1 mouse model of antiphospholipid syndrome cross‐react with oxidized low‐density lipoprotein

Objective. Autoimmunity-prone (New Zealand white X BXSB)F1 ([NZW X BXSB]F1) mice have been shown to be useful as a model of antiphospholipid syndrome with myocardial infarction. The aim of this study was to examine the cross-reactivity of anticardiolipin antibody (aCL) derived from (NZW X BXSB)F1 mice with oxidized low-density lipoprotein (ox-LDL), which is closely associated with atherosclerosis. Methods. Six monoclonal antibodies (MAb) against CL were established from (NZW X BXSB)F1 mice, and reactivity of aCL with ox-LDL was examined by micro–enzyme-linked immunosorbent assay. Results. Higher titers of anti–ox-LDL autoantibodies were found in adult (NZW X BXSB)F1 mice compared with other autoimmunity-prone mouse strains (P < 0.01) or a control strain (P < 0.005). There was a significant positive correlation between titers of aCL and those of anti–ox-LDL in (NZW X BXSB)F1 mice (r = 0.79, P < 0.001). Of the 6 MAb against CL, 2 clones that showed β-glycoprotein 1–dependent reactivity also cross-reacted with ox-LDL. Binding of monoclonal aCL to solid-phase cardiolipin was inhibited by ox-LDL, but not by native LDL. Conclusion. We confirmed that aCL derived from (NZW X BXSB)F1 mice can cross-react with ox-LDL. This result suggests that aCL, which is closely associated with lupus-assocaited thrombosis, may also play an important role in atherosclerotic complications in patients with systemic lupus erythematosus.