Atherosclerosis is a chronic disease that involves a complex interaction of the artery wall and its cellular elements, lipoproteins, and circulating blood elements. Although hypercholesterolemia is a prerequisite for the initiation of atherogenesis, once initiated, the atherosclerotic lesion takes on many of the characteristics of a chronic inflammatory process (1, 2). In particular, there is now strong and growing evidence in hypercholesterolemic animal models that the immune system is specifically activated by atherosclerosis-associated antigens and that both innate and adaptive immunity can significantly modulate subsequent lesion development.
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Joseph L. Witztum (2002) studied this question.
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