We show that the absence of IL-4Rα responsiveness on macrophages only marginally influenced acute bacterial burden, chronic pulmonary pathology and does not influence survival following infection with virulent and hypervirulent strains of Mtb. Taken together, this suggests that IL-4Rα-activated macrophages are not required for TB disease progression since Mtb induces Arg1 production independent of the IL-4Rα signalling pathway. Here, IL4R is linked to tuberculosis.