AFB that reach alveoli are ingested by macrophages. The bacilli impair phagosome maturation, multiply, lyse the macrophages, and spread to regional lymph nodes, from which they may disseminate throughout the body. These initial stages of infection are generally asymptomatic and induce cellular and humoral immunity.

• About 2-4 weeks after infection, a tissue-damaging response resulting from delayed-type hypersensitivity (the basis for tuberculin skin testing [TST]) destroys nonactivated macrophages that contain multiplying bacilli, and a macrophage-activating response activates cells capable of killing AFB. A granuloma forms at the site of the primary lesion and at sites of dissemination. The lesions can then either heal by fibrosis or undergo further evolution. Despite “healing,” viable bacilli can remain dormant within macrophages or in necrotic material for years.
• Cell-mediated immunity confers partial protection against TB. Cytokines secreted by alveolar macrophages contribute to disease manifestations, granuloma formation, and mycobacterial killing.