Mycobacterium tuberculosis(Mtb) is a pathogen that iswidely distributed geographically and continues to be a major threat to world health. Bacterial virulence factors, nutritional state, host genetic condition and immune response play an important role in the evolution of the infection. The genetically diverse Mtb strains from different lineages have been shown to induce variable immune system response. The modern and ancient lineages strains induce different cytokines patterns. The immunity to Mtb depends on Th1-cell activity [interferon-γ(IFN-γ), interleukin-12(IL-12) and tumor necrosis factor-α(TNF-α)]. IL-1β directly kills Mtb in murine and human macrophages. IL-6 is a requirement in host resistance to Mtb infection. IFN-γ, TNF-α, IL-12 and IL-17 are participants in Mycobacterium-induced granuloma formation. Other regulating proteins as IL-27 and IL-10 can prevent extensive immunopathology. CXCL 8 enhances the capacity of the neutrophil to kill Mtb. CXCL13 and CCL19 have been identified as participants in the formation of granuloma and control the Mtb infection. Treg cells are increased in patients with active tuberculosis(TB) but decrease with anti-TB treatment. The increment of these cells causes downregulation of adaptive immune response facilitating the persistence of the bacterial infection. Predominance of Th2 phenotype cytokines increases the severity of TB. The evolution of the Mtb infection will depend of the cytokines network and of the influence of other factors aforementioned. Mycobacterium tuberculosis (Mtb) is a pathogen that is widely distributed geographically and continues to be major thrice to world health. Bacterial virulence factors, nutritional state, host genetic condition and immune response play an important role in the evolution of the infection. The genetically diverse The modern and ancient lineages induced different cytokines patterns. The immunity to Mtb depends on Th1-cell activity [interferon-γ (IFN-γ), interleukin-12 ( IL-1β directly kills Mtb in murine and human macrophages. IL-6 is a requirement in host resistance to Mtb infection. IFN-γ, TNF-α, TNF- IL-12 and IL-17 are participants in Mycobacterium-induced granuloma formation. Other regulatory proteins as IL-27 and IL-10 can prevent extensive immunopathology. CXCL 8 enhances the capacity of the neutrophil to kill Mtb. CXCL13 and CCL19 have bee n identified as participants in the formation of granuloma and control the Mtb infection. Treg cells are increased in patients with active tuberculosis (TB) but decrease with anti-TB treatment. The increment of these cells causes downregulation of adaptive immune response facilitating the persistence of The bacterial infection of Th2 phenotype cytokines increases the severity of TB. The evolution of the Mtb infection will depend on the cytokines network and of the influence of other factors.