Oxidized low-density lipoprotein (oxLDL) interacts in vitro with beta2-glycoprotein I (beta2GPI) via LDL-derived specific ligands forming oxLDL/beta2GPI complexes. Circulating oxLDL/beta2GPI complexes have been demonstrated in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). Autoimmune vascular inflammation and oxidative stress contribute to oxLDL/beta2GPI complex formation. Immunohistochemical staining of atherosclerotic lesions suggest that these complexes are formed in the arterial wall and released into circulation. The demonstration of antibodies to oxLDL/beta2GPI complexes indicates that these complexes are immunogenic, and the coexistence of complexes and antibodies suggest an active pro-thrombotic/pro-atherogenic role in the development of autoimmune vascular complications. Circulating oxLDL/beta2GPI complexes can be measured by ELISA using a monoclonal antibody specific to complexed human beta2GPI to capture beta2GPI bound to oxLDL. An enzyme-conjugated monoclonal antibody to human Apo B 100 allows the specific detection of oxLDL/beta2GPI complexes. OxLDL/beta2GPI complexes were common in SLE and APS patients suggesting an underlying process of inflammation and oxidation. Using oxLDL/beta2GPI complexes as capture antigen, antibodies to oxLDL/beta2GPI can be measured by ELISA. Serum levels of IgG anti-oxLDL/beta2GPI antibodies were significantly higher in SLE patients with APS compared to SLE controls without APS. Further, high titers of these IgG antibodies were observed in APS patients with a history of arterial thrombosis. The presence of circulating oxLDL/beta2GPI complexes and IgG antibodies to these complexes indicates significant vascular injury and oxidative stress as well as an active role in autoimmune-mediated atherothrombosis.