Atherosclerosis as an autoimmune disease: an update

Abstract

Immunoinflammatory processes are discussed increasingly as possible pathogenic factors for the development of atherosclerosis. Here, we summarize the data on which we have built our immunological hypothesis of atherogenesis. This concept is based on the observation that almost all humans have cellular and humoral immune reactions against microbial heat-shock protein 60 (HSP60). Because a high degree of antigenic homology exists between microbial (bacterial and parasitic) and human HSP60, the 'cost' of immunity to microbes might be the danger of cross-reactivity with human HSP60 expressed by the endothelial cells of stressed arteries. Genuine autoimmunity against altered autologous HSP60 might trigger this process also.