Mycobacterium tuberculosis (Mtb) invades the lung via an airborne pathway, and the bacteria reach the lung alveoli and are then engulfed by alveolar macrophages in innate immunity, which uses germline-encoded pattern recognition receptors such as the mannose receptor and Toll-like receptor for recognition of the pathogen. Mtb can survive in phagosomes of macrophages by escaping from lysosomal enzyme and reactive nitrogen intermediate toxicity. Dendritic cells transport Mtb from lung mucosa to draining lymph nodes and present the mycobacterial antigens to CD4+ and CD8+ T cells in adaptive immunity, which uses antigen-specific receptors formed by somatic gene rearrangement. Natural memory T cells such as gammadelta T cells and CD 1-restricted T cells are also stimulated and serve to shape the subsequent development of T-helper 1-dominant immunity, which induces granuloma at the initial focus of infection, is sufficient to prevent acute tuberculosis, but is unable to eradicate the infection completely. Once the host's defense becomes compromised, reactivation of the disease, which is called latent infection with Mtb, occurs. Recent progress in elucidating adaptive immune responses to acute and latent infection with Mtb may lead to the establishment of effective therapeutic and prophylactic approaches for controlling Mtb infection.