Research Information System
TURKIYE KLINIKLERI TIP BILIMLERI DERGISI, vol.28, no.4, pp.508-512, 2008 (SCI-Expanded)
Atherosclerosis is defined as a metabolic and inflammatory disease. Several inflammatory and immunologic factors were established that contributed significantly to atherogenesis. Atherosclerotic lesions contain active immune cells including macrophages and T cells, proinflammatory cytokines and adhesion molecules. Both Immoral and cellular immune mechanisms have a major role in the onset and/or progression of atheromatous lesions. Oxidized low-density lipoprotein (OxLDL), heat shock proteins (HSPs) and beta 2-glycoprotein I (beta 2-GPI) are implicated to be the major antigens in atherogenesis. Circulating autoantibodies (e. g. antiOxLDL, anti beta 2-GPI) against these antigens and/or immune complexes (e.g. OxLDL-antiOxLDL and/or beta 2-GPI-anti beta 2-GPI) within atherosclerotic plaques were detected in both experimental animals and humans. The association of systemic autoimmune inflammatory diseases with atherosclerosis, suggests a similar pathogenic mechanism. The pathogenesis of early or accelerated atherosclerosis in autoimmune diseases is complex and multifactorial. Accelerated atherosclerosis, is a major cause of mortality in systemic lupus erythematosus and antiphospholipid syndrome. Early diagnosis of atherosclerosis, aggressive management of classical risk factors for cardiovascular disease, suppression of systemic inflammation and addition of preventive therapies may reduce the long-term burden of cardiovascular morbidity and mortality in patients with systemic antoimmune disease. In addition, new immunomodulatory treatment strategies are needed.