The cause responsible for the lack of an efficient cell-mediated immunity or a delayed type hypersensitivity to M. leprae in lepromatous patients is poorly understood. But the resistance to M. leprae infection in humans is likely mediated by the activated macrophages to present M. leprae antigen to T cells for cell-mediated immunity. Phenolic glycolipid-I (PGL-I) is a M. leprae-specific antigen and is supposed to play a significant role in the long lasting unresponsiveness in lepromatous leprosy. In this study, IL-1 activities were tested among leprosy patients to evaluate monocyte function and the role of IL-1 in the immunosuppression in leprosy. We found that peripheral blood mononuclear cells (PBMCs) from tuberculoid patients were strongly reactive to M. leprae (mean cpm; 28,853 ± 28,916), but the proliferative responses of PBMCs from lepromatous patients (mean cpm; 6,051 ± 803) were significantly lower. IL-1 concentration in culture supernatant of monocytes from lepromatous patients was similar to that from tuberculoid patients with stimulation of M. leprae (lepromatous: 1,014 ± 637 pg/ml, tuberculoid: 1,012 ± 167 pg/ml) or lipopolysaccharides (IPS) (lepromatous: 3,479 ± 2,188 pg/ml, tuberculoid: 4,246 ± 2,432 pg/ml). The IL-1 concentration is sera from lepromatous patients (42 ± 30 pg/ml) tended to be higher than those from tuberculoid patients (28 ± 69 pg/ml). And there was no significant difference in IL-1 production between peritoneal macrophages from mice sensitized with PGL-1 and those from nonsensitized mice. In conclusion, this study suggests that the immunosuppression in lepromatous patients may not be due to the decreased production of IL-1. And the increased IL-1 activity in sera may affect the inflammatory response of lepromatous patients.