The antifungal macrophages were not inhibited by superoxide dismutase, catalase, dimethyl sulfoxide, or azide. Production of a fungicidal macrophage could also occur after macrophage treatment with conA-stimulated spleen cell supernatants or co-culture of macrophages with lymph-node cells and con A. Earlier work indicating macrophages could be activated for antifungal activity by lymphocyte supernatants has already been cited. In conclusion, the killing mechanism appeared to be related to use of normally available superoxide levels that are not, in unstimulated macrophages, able to develop toxicity for this fungus. Pulmonary macrophages differ functionally, biochemically, and immunologically from other tissue macrophages. The preceding studies relied on polymorphonuclear leukocyte (PMN) elicited chemically from the peritoneal cavity. Another series of experiments showed that the observation of PMN activation resulting from the products of an immune reaction was relevant to a normally circulating and presumably resting stage cell, namely the peripheral-blood PMN.