Immunological mechanisms seem to be potent modulators of the atheroscl
erotic process. The presence of substantial numbers of T-lymphocytes i
n the lesion and local and circulating autoantibodies to plaque compon
ents suggests that a specific immune response is operating. Focal expr
ession of adhesion molecules and local secretion of chemoattractants c
ould mediate the recruitment of inflammatory cells to the lesion. Loca
l cytokine and growth factor networks may operate later, controlling c
ell migration and proliferation. Although it is still important to rea
lize the complexity of these mechanisms, the ongoing characterization
of the molecular mechanisms in atherogenesis may lead to new strategie
s for intervention with the disease process.