Inhibition of atherosclerosis in CD4 T-cell-ablated and nude (nu/nu) C57BL/6 hyperlipidemic mice.

T lymphocytes and monocyte/macrophages are prominent components of atherosclerotic lesions, and many of these cells are activated and secreting cytokines. To determine the role of these cells in the pathogenesis of atherosclerosis, we studied its development in T-cell-deficient mice fed a high fat atherogenic diet. Depleting euthymic mice of their CD4+ lymphocytes by 20 weekly injections of CD4 monoclonal antibodies reduced the mean area of their aortic lesions by approximately 70%.

Chronic alcohol feeding inhibits atherogenesis in C57BL/6 hyperlipidemic mice.

Although there is abundant clinical evidence that the consumption of alcohol (ethanol) in moderate amounts has a protective effect on coronary artery disease, the mechanism of this effect is not understood. The prevailing theory supported by a limited number of clinical and experimental animal studies indicates that the ability of alcohol to elevate serum high-density lipoprotein cholesterol levels is an important mechanism. Although there have been a large number of studies on the effects of alcohol on serum lipoprotein and apolipoproteins on coronary artery disease, there have been very few that have, at the same time, looked directly and systematically at its effects on the histopathological development of atherosclerotic lesions.