The article discusses the cellular immune response to tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb). It highlights the slow induction and expression of the acquired immune response in the lungs, which allows Mtb to establish infection. The interaction between Mtb and the innate immune system, along with auto-regulation of the immune response, results in suboptimal control of bacterial growth. Understanding the factors that mediate the induction, expression, and regulation of the immune response in the lungs is crucial for improving current vaccine strategies. The article also emphasizes the need to induce both known and novel immunoprotective responses without causing immunopathologic consequences. The T cell response is initiated after Mtb infection, with the draining lymph node being the first site of effector function. The slow induction of the immune response is attributed to the low number of bacteria and the limited ability of the lung to initiate cellular responses. The role of dendritic cells in the migration of bacteria to the lymph node is essential for the initiation of the response. The development of cellular responses involves the activation of naive T cells, which then migrate to the primary site of infection. The article also discusses the various subsets of effector T cells, including CD4 T cells producing IFN-γ, and the role of IL-17 and IL-22 in TB. The importance of phagocyte function in controlling Mtb is highlighted, with the role of vitamin D and autophagy in the control of bacterial growth. The role of TLR and pattern recognition receptors in recognizing Mtb as a pathogen is discussed, with the importance of MyD88 in the survival and response to Mtb infection. The article also addresses the role of B cells in the immune response to TB, with evidence suggesting that B cells may play a role in modulating both the inflammatory and cytokine response. The control of T cell responses is discussed, with the potential role of regulatory T cells in modulating the immune response to TB. The article concludes with the importance of understanding the complex interactions between the immune system and Mtb to develop effective vaccines and treatments for TB.The article discusses the cellular immune response to tuberculosis (TB) caused by Mycobacterium tuberculosis (Mtb). It highlights the slow induction and expression of the acquired immune response in the lungs, which allows Mtb to establish infection. The interaction between Mtb and the innate immune system, along with auto-regulation of the immune response, results in suboptimal control of bacterial growth. Understanding the factors that mediate the induction, expression, and regulation of the immune response in the lungs is crucial for improving current vaccine strategies. The article also emphasizes the need to induce both known and novel immunoprotective responses without causing immunopathologic consequences. The T cell response is initiated after Mtb infection, with the draining lymph node being the first site of effector function. The slow induction of the immune response is attributed to the low number of bacteria and the limited ability of the lung to initiate cellular responses. The role of dendritic cells in the migration of bacteria to the lymph node is essential for the initiation of the response. The development of cellular responses involves the activation of naive T cells, which then migrate to the primary site of infection. The article also discusses the various subsets of effector T cells, including CD4 T cells producing IFN-γ, and the role of IL-17 and IL-22 in TB. The importance of phagocyte function in controlling Mtb is highlighted, with the role of vitamin D and autophagy in the control of bacterial growth. The role of TLR and pattern recognition receptors in recognizing Mtb as a pathogen is discussed, with the importance of MyD88 in the survival and response to Mtb infection. The article also addresses the role of B cells in the immune response to TB, with evidence suggesting that B cells may play a role in modulating both the inflammatory and cytokine response. The control of T cell responses is discussed, with the potential role of regulatory T cells in modulating the immune response to TB. The article concludes with the importance of understanding the complex interactions between the immune system and Mtb to develop effective vaccines and treatments for TB.