**5. Conclusion**

Considering the aspects observed during the course of this chapter, macrophages have a crucial role in inducing the immune response to *M. leprae*, and their uptake capacity, phagocytosis, and microbicidal activity may depend on the microenvironment. Macrophages, after the interacting with either the bacilli or its wall components, are able to induce oxidative stress [10–14] and to induce various receptors as scavenger receptors [6, 16, 23, 24, 34, 42–44] and PRR [53–55, 69], leading to the polarization of their response. In an anti-inflammatory profile (M2), this cell induces increased uptake of lipids [21, 22] and Hb-haptoglobin [16, 42], which aid the growth of *M. leprae* by the activation of the enzymes IDO [42, 45], HO-1 [42] and arginase [37]. On the other hand, in a pro-inflammatory and microbicidal profile (M1), the macrophage produces TNF [26, 48], IL-6 [37, 48, 49], and IL-15 [22, 37, 39] besides being able to stimulate T cells to produce IFN-γ [34]. In addition, these M1 macrophages induce autophagy [57, 58], an important process of homeostatic regulation recently described with the immunological role [56], which acts on infection control. Several drugs have been described as autophagy inducers and have been studied as treatment for neurodegenerative diseases [76] and to control of *M. tuberculosis* infection [89]. Autophagy-inducing drugs are promising targets as adjuvants to MDT.
