Macrophages separated from the granulomatous lungs of tuberculous mice had a high amount of cholesterol esters. Resident peritoneal macrophages of normal mice were very low in the ester content. However, when the cells were incubated with mycobacteria in Hanks' solution, the ester content of the mixture increased greatly. Peritoneal macrophages harvested by induction with casein had a much larger amount of cholesterol esters than unstimulated resident cells. When such stimulated macrophages were incubated alone in Hanks' solution, the ester content went down probably due to hydrolysis into free form. This reduction was markedly inhibited by incubation with mycobacteria. These observations at a macrophage level presented a cytological explanation for our previous finding that cholesterol ester content increased in the mouse lungs with the development of granulomatous lesions.