Pulmonary tuberculosis is an infectious disease caused by Mycobacterium tuberculosis (MTB). This microorganism is capable of inducing a delayed hypersensitivity in the lung, with subsequent expression of the disease. This reaction depends on the presence of different cytokines that exert specific functions. To study the variability of different cytokine responses after MTB antigenic challenge, we used antigens derived from MTB to stimulate the monocytes from both normal healthy contact and the patients with active tuberculosis. We found in the resting state monocytes from healthy contact secreted higher amounts of IL-12 than those from patients. After stimulation with MTB antigen, the secretion of IL-12 did not increase in normal healthy contact, but in patients with tuberculosis the secretion increased. After MTB antigen stimulation, monocytes from patients with active tuberculosis secreted a higher amount of TNF-alpha. In summary, the patterns of monocyte-derived cytokine secretion upon mycobacterial antigen challenge were different in these two groups.