TNF-a, an important cytokine for infection control, is involved in the macrophage activation process and is also an important factor related to disease immunopathology. In our study, tuberculosis patients presented significantly higher TNF-a levels than did controls. During treatment, patients presented gradually decreasing levels of this cytokine. Other studies have also shown that individuals with tuberculosis presented elevated TNF-a levels in PBMC culture supernatant compared with controls, and these levels decreased during treatment. In our study, despite the high TNF-a levels in patients at the start of treatment, we observed that this cytokine was not protective at this phase and could have been involved in disease pathogenesis. Because treatment decreased TNF-a levels, we suggest that at lower levels, this cytokine could be involved in protection through the stimulation of pathogenic mechanisms. TNF-a, depending on the concentration produced, could be involved in immunopathological effects such as fever, body weight reduction, tissue necrosis and shock. In our study, pulmonary tuberculosis patients tended to present much lower IL-17 levels at the start of treatment compared with controls. During treatment, production and expression tended to increase. Th17 cells, which are involved in the development of inflammatory and autoimmune diseases, are also involved in protection against certain intracellular pathogens, including M. tuberculosis. However, the exact role of Th17 cells in individuals with pulmonary tuberculosis, mainly during antituberculosis treatment, is not very clear. IL-17 can be SCH727965 induced immediately after pulmonary infection with BCG and can also be detected in the later stages of M. tuberculosis infection. The frequency of Th17 cells in pulmonary TB patients has been reported as significantly lower than in healthy controls and individuals with latent TB. These results suggest that a reduced Th17 response could be associated with the clinical manifestation of pulmonary TB and that this cell subtype might be involved in protection, rather than disease immunopathogenesis. These ideas agree with our findings, as patients at the start of treatment had low IL-17 levels that tended to increase with treatment and pathogen killing. Our results showed that the production of anti-inflammatory cytokines, such as IL-10 and TGF-b, tended to rise during antituberculosis treatment and to diminish at the end of treatment. This phenomenon suggested that these cytokines’ main actuation was at the end of treatment, exerting a regulatory role to control the inflammatory process. Other human studies on tuberculosis have suggested that IL-10 also has a critical role in protecting the host against inflammatory immunopathology. In contrast to our results, studies have shown that patients with a recent diagnosis of pulmonary tuberculosis present higher serum levels of IL-10 than do previously treated or healthy individuals, although treatment reduces the serum concentration of this cytokine.