This brief overview, our concept of an autoimmune pathogenesis of atheroscl
erosis 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 hsp 60 that is expresse
d by endothelial cells that are stressed by classical risk factors for athe
rogenesis such as hypertension, high serum cholesterol levels, components o
f cigarette smoke and other toxins, etc. hsp60 an phylogenetically highly c
onserved and there is an over 55% homology between bacterial hsp60 and the
human homologue forming the basis for this cross-reactivity. As another pos
sibility, the initiation of the disease by a bona fide autoimmune reaction
against chemically altered autologous hsp60 is discussed.