[Immunity, inflammation and atherosclerosis].
Atherosclerotic plaques harbour 3 main cell types: arterial smooth muscle cells, monocyte-macrophages and T-lymphocytes. Together with other morphological characteristics, this feature concurs to the view that plaques are foci of chronic inflammation. The presence of T-cells suggests that immune mechanisms are involved in the development of atherosclerosis. Clinical studies have found correlations between the presence or progression of carotid plaques and the serum concentration of antibodies against oxidized low-density lipoproteins and against heat shock protein HSP-65. Along with other observations, these correlations, if confirmed and extended, may open new avenues to understand the triggering mechanisms of atherosclerosis. However, the available evidence is still insufficient to establish that an autoimmune involvement is a cause rather than a consequence of atherosclerosis.
Capron
L
L
D001161:Arteriosclerosis / Q000209:etiology* / Q000276:immunology; D015551:Autoimmunity / Q000276:immunology; D006360:Heat-Shock Proteins / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000503:physiopathology*; D008077:Lipoproteins, LDL / Q000502:physiology; D013601:T-Lymphocytes
D006360:Heat-Shock Proteins; D008077:Lipoproteins, LDL
Immunité, inflammation et athérosclérose.