Immune cells play an important role in atheromatous plaque formation and progression and in the phase of "active plaque" and of the consequent clinical manifestations. Endothelial dysfunction is the first determinant step in atherogenesis by inducing the alteration of vasodilating and antithrombotic properties of the endothelium and of its permeability to lipoproteins. Circulating monocytes are recruited and internalized and lipoproteins are stored in the subendothelial area where they undergo oxidation (oxidized LDL) and are removed by macrophages by means of non-autoregulated scavenger receptors (foam cells). Foam cells are able to express surface receptors and to produce soluble mediators (interleukin-1, tumor necrosis factor-alpha, monocyte chemotactic protein 1) which attract other monocytes, activate endothelial cells and smooth muscle cells. Lymphocytes too are present in these first stages of atherogenesis. If the injurious agents are not removed or nullified by the inflammatory response and the inflammation progresses, the response changes from a protective to an injurious response. Recruitment of monocytes and lymphocytes occurs as a result of the up-regulation of adhesion molecules on both the endothelium and the leukocytes and the plaque progresses to an advanced lesion. Finally the activation of monocytes and T cells induces the plaque activation and rupture in presence of inducing agents such as oxidized LDL. CD4 lymphocytes are common components of atheroma and are mainly localized at the sites of rupture in strict contact with macrophages and smooth muscle cells which express activation surface molecules and which are able to process and to present the antigen to T cells. Activated lymphocytes produce proinflammatory cytokines as interferon-gamma which is able to amplify the inflammatory response but also interleukin-10 which seems to possess a regulatory effect. Activated macrophages release metalloproteinases and other proteolytic enzymes which cause degradation of the matrix, thinning of fibrous cap and plaque destabilization. Both T cells and macrophages produce cytotoxic factors which contribute to the apoptosis. The process may be potentiated by the activation of platelets, tissue factor, coagulation-fibrinolytic system which can contribute to thrombus formation, plaque rupture and artery occlusion.