Immunopathogenesis of tuberculosis: cellular mechanisms and immune modulation.

Tuberculosis (TB) is a worldwide zoonotic disease caused by bacteria members of the Mycobacterium tuberculosis complex (MTC), which affects a wide range of domestic and wildlife species, as well as humans. TB is characterized as a chronic pulmonary infection, primarily affecting the lungs and local lymph nodes (LNs), causing significant respiratory and immunosuppression problems. MTC members have the capability to survive in the host by evading the immune system's killing mechanisms and persisting within macrophages. This chronic antigenic stimulation promotes the formation of a complex, organized tissue structure known as a tuberculous granuloma, which is a defining cellular response to mycobacteria infections, and is composed of a compact aggregate of immune cells, whose functions are modulated by cytokines. The immune response against TB is complex and nowadays is not completely understood; therefore, the study of its immunopathogenesis becomes essential for evaluating immune-mediated response against mycobacterial infections, and consequently, develop strategies to control and eradicate the propagation of this disease in animals and humans. The aim of this work was to review the literature on key cell populations and immunological markers involved in the formation and development of granulomas in the lungs of humans and animals, and to discuss their potential use in evaluating the efficacy of novel vaccine candidates ‒ a tool that could contribute to TB control.