Lopez Luis R, Buckner Tammy R, Hurley Beth L, Kobayashi Kazuko, Matsuura Eiji
Corgenix Inc., Broomfield, CO 80020, USA.
Ann N Y Acad Sci. 2007 Aug;1109:303-10. doi: 10.1196/annals.1398.036.
The immunolocalization of oxidized low-density lipoproteins (ox-LDL), beta2-glycoprotein I (beta(2)GPI), CD4(+)/CD8(+) immunoreactive lymphocytes, and immunoglobulins in atherosclerotic lesions strongly suggested an active participation of the immune system in atherogenesis. Oxidative stress leading to ox-LDL production is thought to play a central role in both the initiation and progression of atherosclerosis. ox-LDL is highly proinflammatory and chemotactic for macrophage/monocyte and immune cells. Enzyme-linked immunosorbent assays (ELISAs) to measure circulating ox-LDL have been developed and are being currently used to assess oxidative stress as risk factor or marker of atherosclerotic disease. ox-LDL interacts with beta(2)GPI and circulating ox-LDL/beta(2)GPI complexes have been demonstrated in patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS). It has been postulated that beta(2)GPI binds ox-LDL to neutralize its proinflammatory and proatherosclerotic effects. Because beta(2)GPI is ubiquitous in plasma, its interaction with ox-LDL may mask oxidized epitopes recognized by capture antibodies potentially interfering with immunoassays results. The measurement of ox-LDL/beta(2)GPI complexes may circumvent this interference representing a more physiological and accurate way of measuring ox-LDL.
氧化型低密度脂蛋白(ox-LDL)、β2糖蛋白I(β(2)GPI)、CD4(+)/CD8(+)免疫反应性淋巴细胞以及免疫球蛋白在动脉粥样硬化病变中的免疫定位强烈提示免疫系统在动脉粥样硬化形成过程中积极参与。导致ox-LDL产生的氧化应激被认为在动脉粥样硬化的起始和进展中都起着核心作用。ox-LDL具有高度促炎作用,并且对巨噬细胞/单核细胞和免疫细胞具有趋化作用。已经开发出用于测量循环ox-LDL的酶联免疫吸附测定(ELISA),目前正用于评估氧化应激作为动脉粥样硬化疾病的危险因素或标志物。ox-LDL与β(2)GPI相互作用,并且在系统性红斑狼疮(SLE)和抗磷脂综合征(APS)患者中已证实存在循环ox-LDL/β(2)GPI复合物。据推测,β(2)GPI结合ox-LDL以中和其促炎和促动脉粥样硬化作用。由于β(2)GPI在血浆中普遍存在,其与ox-LDL的相互作用可能会掩盖捕获抗体识别的氧化表位,从而可能干扰免疫测定结果。测量ox-LDL/β(2)GPI复合物可能会规避这种干扰,这代表了一种更符合生理且准确的测量ox-LDL的方法。