A group of anticardiolipin antibodies (aCL) require beta 2-glycoprotein I (beta 2GPI) to recognize their target, which might be located on endothelial cells (EC) and/or platelets. Following incubation with epithelial cells, 13 of 30 lupus sera retained EC-reactive antibodies of the IgG, IgA and IgM isotypes. Associated aCL and anti-phosphatidylethanolamine antibodies were partly absorbed on eC as well as EC. The former antibodies were more efficiently removed in the presence than in the absence of the latter. The presence of beta 2GPI in the affinity-purified aCL preparations may explain their binding to EC, as this cross-reaction was abrogated by the removal of the cofactor and restored by its re-introduction. Seventy four per cent of EC were faintly stained with polyclonal or monoclonal antibody directed to the cofactor. The beta 2GPI mediated aCL binding to EC membranes could this be influential in the development of thrombosis and/or thrombocytopenia in aCL-positive patients.

Twenty years have passed since the original description of the anti-endothelial cell antibodies (AECA). It is widely acknowledged that the presence of circulating autoantibodies against endothelial cells surface antigens, found in a number of patients with connective tissue disease and vasculitis, is one of the driving mechanisms for the observed vascular injury and might be an important factor in initiating the pathogenesis of vascular abnormalities. AECA data regarding the prevalence, technical problems, presence with other autoantibodies, antigen distribution and immune endothelial cell injury associated with these autoantibodies, requires standardization for determining the precise pathophysiologic and immunologic role of anti-endothelial cell antibodies.

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