This brief overview, our concept of an autoimmune pathogenesis of atherosclerosis is summarized. In principle, we postulate that we may have to "pay" for our protective immunity against microbial heat-shock protein 60 (hsp60) with the danger of a cross-reactivity with our own hsp60 that is expressed by endothelial cells that are stressed by classical risk factors for atherogenesis such as hypertension, high serum cholesterol levels, components of cigarette smoke and other toxins, etc. hsp60 are phylogenetically highly conserved and there is an over 55% homology between bacterial hsp60 and the human homologue forming the basis for this cross-reactivity. As another possibility, the initiation of the disease by a bona fide autoimmune reaction against chemically altered autologous hsp60 is discussed.