Research in recent years has resulted in an increased understanding of the molecular mechanisms in the development of inflammatory processes. In atherosclerosis, focal expression of key adhesion molecules has been detected which may mediate the recruitment of mononuclear cells to the plaque. Local cytokine production could account for further cell migration and proliferation. The presence of substantial numbers of T lymphocytes in the plaque and local and circulating autoantibodies to modified lipoproteins suggest that T and B lymphocyte responses may play important roles in these processes.