|
 |
|||||||||||||||||||
|
|||||||||||||||||||
|
|||||||||||||||||||
 |
 |
|
|
a Department of Cell Chemistry, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan b Corgenix Inc., Broomfield, Colorado 80020, USA
Key Words: oxidized low-density lipoprotein • antiphospholipid syndrome •  2-glycoprotein I
Address for correspondence: Eiji Matsuura, Ph.D., Department of Cell Chemistry, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. Voice: +81-86-235-7402; fax: +81-86-235-7404. eijimatu{at}md.okayama-u.ac.jp
Macrophage uptake of oxidized LDL (oxLDL) plays a critical role in early stages of atherosclerosis. We previously reported that oxLDL forms stable complexes with
2-glycoprotein I (2GPI), and that these complexes were frequently present in the sera of patients with systemic lupus erythematosus (SLE) and/or antiphospholipid syndrome (APS). oxLDL/2GPI complexes were shown to be antigenic targets for autoantibodies present in APS. To understand the role of autoantibodies in accelerated atherosclerosis of SLE and APS, we investigated the binding characteristics of 2GPI and oxLDL to mouse macrophages, and the effect of anti-2GPI and anti-oxLDL autoantibodies on this macrophage binding. IgM anti-oxLDL antibody (derived from Apoe–/– mouse) showed inhibitory effect on oxLDL binding to macrophages. Although 2GPI partly inhibited oxLDL binding to macrophages, IgG anti-2GPI autoantibody (derived from APS model mouse) showed pro-atherogenic property by promoting the binding of oxLDL/2GPI to macrophages.
|
 |
 |
