Immune-mediated mechanisms of endothelial damage in atherosclerosis.

The endothelium of the vessel wall as a barrier between blood and the subendothelial matrix proteins is essential for preventing thrombus formation and subsequent atherosclerosis development. Atherosclerosis is an inflammatory disease in which immune and autoimmune mechanisms are involved. Recently, it was demonstrated that endothelial cells in the vessel wall can be damaged not only by classic risk factors, such as hyperlipidemia, smoking and disturbed blood flow, but also (auto)immune reactions to autoantigens present in the cell surface, among which heat shock protein 60 (HSP60) was mostly studied. HSP60 normally located in mitochondria can be translocated into the cell member in response to stress stimuli. Meanwhile, autoantibodies against HSP60 are present in most subjects, especially patients with heart attack and stroke. These autoantibodies may bind to HSP60 expressed in endothelial cells resulting in the cell damage, subsequently initiating the formation of atherosclerotic lesions. Based on the recent progress in the research field, the present review will update the mechanisms of immune response to endothelial cells by which cell damage can initiate the development of atherosclerosis.