Immune mechanisms in atherosclerosis : Coronary Artery Disease (original) (raw)

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Department of Clinical Chemistry, Gothenburg University, Gothenburg, Sweden.

Abstract

Atherosclerosis represents one of the main causes of death and disease in industrialized societies. Patho-genetically, it is characterized by a focal, slow, and progressive accumulation of cells, extracellular matrix, and lipid in the intima of medium-sized and large arteries. The resulting luminal occlusion and thrombosis lead to fatal or severely disabling clinical manifestations such as myocardial and cerebral infarction.

Large epidemiological studies have provided important information on atherosclerosis, which has been used in attempts to prevent the disease. It has been estimated, however, that only approximately 50% of the incidence of cardiovascular disease can be explained by the major risk factors. Consequently, there is room for substantial, as yet unknown, contributing factors. Furthermore, epidemiology has not provided an understanding of the pathophysiological mechanisms of atherosclerosis. With the exception of a small number of genetic disorders of lipid metabolism, the cause and molecular and cellular pathogenesis of atherosclerosis remain unclear.

The growing realization of the presence of T lymphocytes in the plaque [1] and the finding of antibody responses to plaque constituents has reawakened the interest in inflammatory and immune components in atherogenesis. Much of the current interest in atherosclerosis research is focused on cell recruitment and cellular communication in the evolving atherosclerotic plaque. The presence of activated T cells and signs of T cell cytokine secretion in atherosclerotic lesions suggest a role for local T cell responses in atherogenesis. Several studies demonstrating the presence of autoantibodies to modified lipoproteins or heat shock proteins indicate that atherosclerosis may also involve B cell responses. The present review aims to summarize and discuss recent progress in this area.