• Ilir I Cinoku, Clio P Mavragani, and Haralampos M Moutsopoulos.
• Department of Physiology, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
• Eur. J. Clin. Invest. 2020 Feb 1; 50 (2): e13195.

AbstractAtherosclerosis has long been considered as a lipid storage disease. Recent data suggest that autoimmune mechanisms seem to be involved in the pathophysiology of atherosclerosis. The presence of activated endothelial vascular cells, neutrophils, macrophages, T and to a lesser extent B cells in atherosclerotic plaques, together with the proinflammatory cytokine burden suggest mobilization of both innate and adaptive immune pathways in atherosclerosis pathobiology. The development of antibodies to oxidized low-density lipoprotein (ox-LDL), the experimental induction of atherosclerosis either via the transfer of T cells or immunization with autoantigens such as β2 glycoprotein Ι (β2-GPI) and heat shock proteins (HSP) further support the autoimmune nature of atherosclerosis. However, classical immunosuppressive and immune-modulatory drugs, successfully used in the therapy of autoimmune rheumatic diseases have shown limited benefits so far in the treatment of atherosclerosis.© 2019 Stichting European Society for Clinical Investigation Journal Foundation.

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