Recent studies have revealed that atherosclerosis bears several simila
rities to chronic inflammation. One of the earliest events in both hum
an and experimental atherosclerosis is adhesion of monocytes and T lym
phocytes to endothelial surface followed by their migration into the i
ntima. This intimal recruitment of blood derived cells, coupled with t
he enhanced endothelial permeability to plasma proteins, indicates a p
otential role for inflammatory mechanisms in early atherogenesis. Colo
calization of T lymphocytes and macrophages in all stages of human ath
erosclerosis, from grossly normal prelesional intima to fully advanced
atheromatous plaques, and expression of cytokines and MHC class II an
tigens by many types of cells of the lesion provide further evidence t
hat atherosclerosis has both the inflammatory and immune nature. The p
resence of T lymphocytes and macrophages in pairs with a close contact
to each other suggests that cognate cell to cell interaction also pla
ys a pivotal role in the pathogenesis of atherosclerosis. It seems con
ceivable that the T lymphocyte-macrophage interaction particularly tak
es place in the areas where atherosclerotic lesions are in progress or
being active. The pathogenic potentials of immunologic factors are fr
uitful subjects for further investigation.