Autoantibody-mediated atherosclerosis

β2-Glycoprotein I (β2-GPI) is a major antigen for antiphospholipid antibodies (aPL) present in patients with antiphospholipid syndrome (APS). Oxidized low-density lipoprotein (oxLDL) is subsequently targeted by β2-GPI and anti-β2-GPI autoantibodies. Ligands specific for β2-GPI derived from oxLDL have been characterized as oxidized forms of cholesteryl linoleate, such as 7-ketocholesterol-9-carboxynonanoate, i.e. 9-oxo-9-(7-ketocholest-5-en-3β-yloxy) nonanoic acid, (namely oxLig-1). The in vitro phenomenon that it is significantly increased in binding of oxLig-1 containing liposomes to macrophages via an interaction with β2-GPI and an anti-β2-GPI autoantibody (via the Fcγ receptor) may propose a novel mechanism on ‘autoantibody-mediated athrosclerosis’. Furthermore, autoantibodies against a complex of β2-GPI and oxLig-1 are detected in sera of APS patients and appearance of the antibodies is associated with episodes of thrombosis, especially, arterial thrombosis. Thus, autoimmune atherogenesis linked to β2-GPI interaction with oxLDL and autoantibodies may be present in APS.