The immune system is involved at all stages of the atherosclerotic disease process. Innate immunity, represented by macrophages and other cells, is directly activated by microbial components and possibly also by autologous lipids and proteins. It elicits inflammatory activity, which is a key component of the atherosclerotic lesion. Adaptive immunity is initiated by recognition of disease-related antigens, which include oxidatively modified lipoproteins, heat shock proteins and microbial macromolecules. In the artery wall, adaptive immune recognition mainly leads to Thl effector responses, which are characterized by secretion of proinflammatory cytokines and by activation of macrophages and vascular cells. Therefore, both the innate and adaptive arms of the immune system lead to inflammation in the developing atherosclerotic lesion. Interestingly, several effector pathways of cellular as well as humoral immunity tend to counteract proatherogenic, proinflammatory immunity. The notion that immunity plays an important role in the development of atherosclerosis has focused attention on a number of potential novel targets for intervention based on modulation of such immune responses.