The importance of the immuno-inflammatory processes involved in the pathogenesis of atherosclerosis has been reconsidered since the various cellular components of the atherosclerotic plaque were more precisely characterized. Macrophages and T lymphocytes, as well as endothelial and smooth muscle cells are involved in the formation of the fibrolipidic lesion. This is suggestive of a delayed-type hypersensitivity reaction, with oxidized low-density lipoproteins (LDL) as possible antigenic stimulus. Cytokines, which are mediators of the immuno-inflammatory response, are locally expressed in the atherosclerotic plaque; they coordinate cell interactions and modulate the functions of vascular cells.