Elsevier

Atherosclerosis

Volume 19, Issue 3, May–June 1974, Pages 353-367
Atherosclerosis

Immunity and inflammation in the pathogenesis of atherosclerosis: A review

https://doi.org/10.1016/S0021-9150(74)80001-8Get rights and content

Summary

This paper reviews and discusses the evidence that immune mechanisms and inflammation may be involved in the pathogenesis of atherosclerosis and ischaemic vascular disease (I.V.D.). Thrombosis, lipid imbibition and arteritis are existing theories of the origin of atherosclerosis. The latter two theories can be combined, as increase of endothelial permeability due to inflammation may lead to increased lipid entry. The development of rabbit atherosclerosis can be inhibited by anti-inflammatory and immunosuppressive durgs. Arteritis can be produced experimentally by immune complex disease (serum sickness), and when combined with lipid feeding leads rapidly to atherosclerosis. The occurrence of immune-complex induced atherosclerosis in man is suggested by the finding of increased levels of milk antibodies in patients with myocardial infarction; evidence has been obtained for the absorption of undigested dietary proteins. An increased incidence of allergy to tobacco protein was found in smokers with I.V.D. The possibility that abnormalities in platelet and red cell behaviour in patients with I.V.D. are due to immune complexes is considered. The action of the complexes on platelets may promote thrombosis. Hyperlipidaemia has been produced by antigenic challenge and by certain autoantibodies. Autoantibodies to arterial tissues have been found in I.V.D. and the involvement of these and cellmediated immune mechanisms in the pathogenesis of the atherosclerotic plaque are discussed. Inflammation may produce a self perpetuating process by which deposits of lipid cause further lipid entry.

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    R. N. Poston thanks the British Medical Association and the British Heart Foundation for the generous provision of research fellowships.

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