Mycobacterium tuberculosis (Mtb), an intracellular pathogen, is phagocytosed by alveolar macrophage but it is not digested; it survives, proliferates and establishes Mtb infections. The long-term survival mechanism of Mtb is not yet clear. The host's immune response to Mtb is mainly mediated by a Toll-like receptor 2 (TLR2) in macrophages. In the early stage of the immune response by macrophage activation through TLR2, the proliferation of Mtb is suppressed and there is a direct bactericidal effect or induction of apoptosis in infected macrophages. This indicates that TLR2 signaling functions as a defense system against Mtb infection. However, TLR2 signaling from Mtb also appears to be part of the Mtb strategy to escape immune responses by macrophages, such as has been observed when there has been a decrease in MHC-II expression or antigen-processing activity. TLR signaling is reported both to be and not be involved in the maturation of phagosomes, indicating the possibility of contrary influences. In this review, we summarize immune responses of macrophages through TLR2 in Mtb infection, its involvement in phagosome maturation and we describe survival strategies of Mtb through TLR2 signaling.