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Atherosclerosis: Beyond the lipid storage hypothesis. The role of autoimmunity
Author(s) -
Cinoku Ilir I.,
Mavragani Clio P.,
Moutsopoulos Haralampos M.
Publication year - 2020
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/eci.13195
Subject(s) - autoimmunity , immunology , immune system , proinflammatory cytokine , medicine , heat shock protein , autoimmune disease , inflammation , antibody , biology , biochemistry , gene
Atherosclerosis 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.