Immunocompetent cells infiltrate atherosclerotic plaques of all stages. Plaque-infiltrating T-cells recognize oxidized LDL and heat shock proteins and this elicits antibody responses that have been proposed as markers of disease activity. Cytokines secreted by activated T-cells may control macrophage activation, scavenger receptor expression and metalloproteinase secretion. Furthermore, cytokines secreted by T-cells and macrophages modulate smooth muscle proliferation, nitric oxide production and apoptosis, and induce endothelial activation. However, both positive and negative signals, as well as feedback loops, may be induced because of the complexity of the immune system. The possibility that some of these signals may be protective against atherosclerosis is currently under investigation in several laboratories. Recent studies in experimental animals show that immunomodulation affects the development of plaques and that immunization with oxidized LDL can inhibit lesion formation. This review provides a brief overview of cellular immunology and an analysis of its potential role in atherogenesis.