Recent studies have revealed that atherosclerosis bears several similarities to chronic inflammation. One of the earliest events in both human and experimental atherosclerosis is adhesion of monocytes and T lymphocytes to endothelial surface followed by their migration into the intima. This intimal recruitment of blood derived cells, coupled with the enhanced endothelial permeability to plasma proteins, indicates a potential role for inflammatory mechanisms in early atherogenesis. Colocalization of T lymphocytes and macrophages in all stages of human atherosclerosis, from grossly normal prelesional intima to fully advanced atheromatous plaques, and expression of cytokines and MHC class II antigens by many types of cells of the lesion provide further evidence that atherosclerosis has both the inflammatory and immune nature. The presence of T lymphocytes and macrophages in pairs with a close contact to each other suggests that cognate cell to cell interaction also plays a pivotal role in the pathogenesis of atherosclerosis. It seems conceivable that the T lymphocyte-macrophage interaction particularly takes place in the areas where atherosclerotic lesions are in progress or being active. The pathogenic potentials of immunologic factors are fruitful subjects for further investigation.