In conclusion, we demonstrate that despite a robust increase in IDO-1 expression, activation of tryptophan metabolism in infected macrophages and a role for DC-derived IDO-1 in regulating T cell responses in vitro, immune control of M. tuberculosis in macrophages occurs independently of IDO-1 and IDO-1 is redundant for regulating control of M. tuberculosis infection in a mouse model of tuberculosis. Here, IDO1 is linked to tuberculosis.