Soluble interleukin-2 receptor- α (IL-2R α ) has been reported to be increased in the sera of patients with advanced tuberculosis, and levels decline after therapy in accordance with improvement of radiologic findings. We investigated expression of the IL-2R α in bronchoalveolar lavage (BAL) cells in active pulmonary tuberculosis, and evaluated the mechanism Mycobacterium tuberculosis induces in the IL-2R α using the THP-1 mononuclear phagocyte cell line. We found IL-2R α expression to be increased in BAL cells from involved sites of active pulmonary tuberculosis. Expression of the α -chain of IL-2R α on peripheral blood monocytes (PBM) was induced by M. tuberculosis by flow cytometry evaluation. Northern analysis demonstrated increased IL-2R α gene expression after stimulation with M. tuberculosis which was further induced by interferon- γ (IFN- γ ). The IL-2R α promoter containing the nuclear factor kappa B (NF- κ B) site was transcriptionally induced by M. tuberculosis and this NF- κ B site could confer inducibility to a heterologous herpes thymidine kinase (TK) promoter by M. tuberculosis. Electrophoretic mobility shift assays (EMSAs) revealed specific binding of nuclear protein to the NF- κ B site upon induction with M. tuberculosis. Using antibodies against the p50 and p65 subunits of NF- κ B in EMSAs, the involvement of both p50 and p65 proteins was further demonstrated. Functional expression of the IL-2R α on mononuclear phagocytes in M. tuberculosis infection may play an important immunomodulatory role in the host response.