Autoantibody-mediated atherosclerosis.
Beta2-glycoprotein I (beta2- 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 beta2- GPI and anti-beta2-GPI autoantibodies. Ligands specific for beta2- 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-3beta-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 beta2- GPI and an anti-beta2-GPI autoantibody (via the Fcgamma receptor) may propose a novel mechanism on 'autoantibody-mediated atherosclerosis'. Furthermore, autoantibodies against a complex of beta2- 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 beta2- GPI interaction with oxLDL and autoantibodies may be present in APS.[1]References
- Autoantibody-mediated atherosclerosis. Matsuura, E., Kobayashi, K., Koike, T., Shoenfeld, Y. Autoimmunity reviews. (2002) [Pubmed]
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