Mast cells are characterized by numerous granules released extracellularly in response to stimuli, e.g. IgE and complement. These cells are believed to be crucial in the development of certain inflammatory or immune-mediated diseases, such as allergy and dermatitis, and it has recently been demonstrated that a large number of mast cells are present in atherosclerotic lesions. Atherosclerosis bears several similarities to chronic inflammation, characterized by T cell and monocyte infiltration, immunoglobulin-complement deposition, and lipid accumulation. The presence of mast cells in atherosclerotic lesions could be significant because they can release large amounts of chemotactic agents, inflammation activators, and granule remnants, and they may be responsible for mononuclear cell recruitment and smooth muscle cell proliferation. Furthermore, granule remnants nonspecifícally bind to low-density lipoproteins, which can be phagocytosed by macrophages to form foam cells, a major cellular component of the early stage of atherosclerotic lesions. Thus, further elucidation of the role of mast cells in quantitative studies could enhance our understanding of the mechanism of atherogenesis, and may lead to new therapeutic strategies for atherosclerosis.