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Mycobacterium tuberculosis  ( M. tuberculosis ), an intracellular pathogenic Gram-positive bacterium, is the cause of tuberculosis (TB), a major worldwide human infectious disease. The innate immune system is the first host defense against  M. tuberculosis . The recognition of this pathogen is mediated by several classes of pattern recognition receptors expressed on the host innate immune cells, including Toll-like receptors, Nod-like receptors, and C-type lectin receptors like Dectin-1, the Mannose receptor, and DC-SIGN.  M. tuberculosis  interaction with any of these receptors activates multiple signaling pathways among which the protein kinase C, the MAPK, and the NFκB pathways have been widely studied. These pathways have been implicated in macrophage invasion,  M. tuberculosis  survival, and impaired immune response, thus promoting a successful infection and disease. Interestingly, the Wnt signaling pathway, classically regarded as a pathway involved in the control of cell proliferation, migration, and differentiation in embryonic development, has recently been involved in immunoregulatory mechanisms in infectious and inflammatory diseases, such as TB, sepsis, psoriasis, rheumatoid arthritis, and atherosclerosis. In this review, we present the current knowledge supporting a role for the Wnt signaling pathway during macrophage infection by  M. tuberculosis  and the regulation of the immune response against  M. tuberculosis . Understanding the cross talk between different signaling pathways activated by  M. tuberculosis  will impact on the search for new therapeutic targets to fuel the rational design of drugs aimed to restore the immunological response against  M. tuberculosis .

Activation of the Wnt Pathway by Mycobacterium tuberculosis: A Wnt–Wnt Situation