Indeed, because the activity of unrestrained TNF and IFN-γ can be detrimental to the host under conditions of infection or microbial colonization, including during M. tuberculosis infection, various mechanisms are in place to prevent immunopathology, including those mediated by Foxp3+ regulatory T cells [16, 90, 91, 93] and IL-10 [14, 58–60, 74]. Here, IFNG is linked to infection.