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OxLDL/β2-glycoprotein I complex as a pro-atherogenic autoantigen. Is atherosclerosis an autoimmune disease?


Authors: Pavel Kraml
Authors‘ workplace: Centrum pro výzkum diabetu, metabolizmu a výživy II. interní kliniky 3. LF UK a FN Královské Vinohrady, Praha
Published in: Vnitř Lék 2016; 62(Suppl 4): 48-51
Category: Reviews

Overview

Oxidation of atherogenic low-density lipoproteins (LDL) plays a key role in the pathogenesis of atherosclerosis. Oxidation stress and inflammation are closely interrelated and they can potentiate one another. In the subendothelial space of the arterial intima, monocytes/macrophages become activated and phagocyte oxidized LDL (oxLDL) via scavenger receptors. It has been demonstrated that oxLDL forms complex with plasma β2-glycoprotein I (β2GPI) and becomes autoantigenic triggering synthesis of specific antiphosholipid antibodies. It has been documented that oxLDL/β2GPI in immune complex with IgG autoantibody is internalized by macrophages through the Fcγ receptor. Increased levels of oxLDL/β2GPI were first observed in patients with systemic lupus erythematodes (SLE) and antiphospholipid syndrome (APS), further in individuals with coronary heart disease (CHD) and type 2 diabetes mellitus (DM2T). In a prospective study, initial plasma concentrations of oxLDL/β2GPI correlated with the number and severity of cardiovascular events in patients with chronic CHD over a 2-year period.

Key words:
atherosclerosis – β2-glycoprotein I – inflammation – oxidative stress – oxLDL


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Diabetology Endocrinology Internal medicine

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