The modern view of atherosclerosis is of a chronic inflammatory disorder. I
n accord with this paradigm, the process of uninhibited influx of fat to th
e vessel wall results from an 'adequate' response to various forms of injur
y (i.e. turbulence, infections, modified lipoproteins). This idea has been
further extended by several groups, to assume that the atherosclerotic lesi
on can be the target of an autoimmune mediated attack. According to this hy
pothesis, the site of initiation of the plaque should bear/express the targ
et autoantigen, whereas concomitantly a respective immune response is gener
ated in the periphery. The examples illuminating this notion are beta 2GPI
as a target autoantigen, HSP60/65 an oxidized-LDL.
Herein we present evidence to support the involvement of autoimmune mechani
sms in atherogenesis based on the experience from experimental models and h
uman studies.