Human atherosclerosis is a long-standing chronic disease that begins in childhood but does not become manifest clinically until middle age or later. Various kinds of arterial injury, including those by hypercholesterolemic, immunologic, viral, chemical, and mechanical factors, participate in the initiation and progression of atherosclerosis. Macrophages, smooth muscle cells, endothelial cells, and T lymphocytes are the most frequent cell types present in atherosclerotic lesions. Interactions among these cellular components within the arterial wall are believed to be essential in the development and progression of atherosclerosis.'%* It is conceivable that, since many individuals develop atherosclerosis in the absence of known risk factors such as altered blood lipoproteins and high blood pressure, individual susceptibility to atherosclerosis may reside in the response of vascular cells to known and currently unknown risk factors.

Recent immunohistological invcstigations have unequivocally shown that in addition to macrophages, comparably a large number of T lymphocytes are present in human atherosclerotic The selective accumulation of T lymphocytes and macrophages in the arterial intima may imply a possible contribution of cellmediated immune reactions in human atherogenesi~,~,~ since their interaction and subsequent cytokine production are known to be involved in the pathogenesis of a variety of human diseases. To verify whether such events occur at any stage and any site of human atherosclerosis, the following overview briefly outlines our observations on the evolutional changes of human atherosclerosis including the grossly normal intima of children, fatty streaks, and atheromas. We will also provide a brief summary of the study pursued in the diet-induced rat model to investigate the nature of the cells accumulated in the early phase of lcsion development.