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Mycobacterium tuberculosis (M. tuberculosis), which is the etiological agent of tuberculosis (TB), has become one of the most successful pathogens in human history with its ability to cause active/latent infection even in the face of a perfectly functioning immune system, thanks to its mutual evolution with the host cell over thousands of years. While one-fourth of the world’s population are estimated to be infected by M. tuberculosis, only 5-15% of this population fall ill with active TB disease throughout life. The main reason for this situation is the effective mechanisms of host immunity. After the TB bacillus is taken into the body by inhalation, it first encounters the natural immune cells. Acquired immunity develops against bacilli that cannot be eliminated by natural immunity. M. tuberculosis has developed quite a variety of strategies to evade the immune system. These strategies include escape from pathogen recognition receptors, inhibition of phagolysosome formation, inhibition of apoptosis and autophagy, immune escape with granuloma formation, inhibition of oxidative stress, and reactive oxygen and reactive nitrogen intermediates. Unraveling the mechanisms by which M. tuberculosis alters or modulates host immune function is probably of great importance for the development of more effective new vaccines and immunotherapy against TB. In this review, we aim to reveal new developments about the host immune response against M. tuberculosis and the escape mechanisms of bacillus from this response. [ABSTRACT FROM AUTHOR]