Immunoinflammatory processes are discussed increasingly as possible pathoge
nic 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 cellul
ar and humoral immune reactions against microbial heat-shock protein 60 (HS
P60). Because a high degree of antigenic homology exists between microbial
(bacterial and parasitic) and human HSP60, the 'cost' of immunity to microb
es might be the danger of cross-reactivity with human HSP60 expressed by th
e endothelial cells of stressed arteries. Genuine autoimmunity against alte
red autologous HSP60 might trigger this process also.