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Mycobacterium tuberculosis, the causative agent of tuberculosis is a facultative intracellular pathogen that infects and resides in humans and is a leading infectious cause of death in many parts of the world with a worrying increase in transmission and resistance to drugs. Surfactant proteins A and D (SP-A and -D) play a role in many acute bacterial, viral, and fungal infections and in acute allergic responses. In vitro, human SPs bind Mycobacterium tuberculosis and alter human and rat macrophage-mediated functions. Here we report the roles of SP-A and SP-D in M. tuberculosis infection following aerosol challenge of SP-A-, SP-D-, and SP-A/-D-deficient mice. These studies surprisingly identified no gross defects in uptake or immune control of M. tuberculosis in SP-A-, SP-D-, and SP-A/-D- deficient mice. While both SP-A- and SP-D-deficient mice exhibited evidence of immunopathologic defects, the CD11b high CD11c high dendritic cell populations and the gamma interferon (IFN-γ)-dependent CD4+ T cell response to M. tuberculosis were unaltered in all genotypes tested. Together, these data indicate that SP-A and SP-D are dispensable for immune control of M. tuberculosis in a low-dose, aerosol challenge, murine model of tuberculosis (TB). This pathogen is generally transmitted by inhalation of infectious aerosols into the lung with deposition in the terminal bronchioles and alveoli. Most affected persons stand an effective immune response that might controls this pathology but does not totally eradicate the primary tuberculosis infection and the reactivation of persistent M. tuberculosis later in life occur frequently in active tuberculosis cases . Many studies are still running up in order to better understand the interactions between M. tuberculosis and the immune environment of the lung. In this review, we describe initial interactions between the lung environment and M. tuberculosis and we summarize the normal surfactant turnover by alveolar macrophages and AEC II in to the uptake of M. tuberculosis in alveolar epithelial cells and macrophages during the innate immune response followed by the T cells initiation of the adaptive immunity in the lung.