IL4R and tuberculosis: Experiments with the use of mice with IL-13 overexpression (IL-13tg) and with the absence of IL-4Rα (IL-4Rα−/−) revealed that deletion of IL-4Rα abrogates the increased susceptibility of Mtb-infected IL-13tg mice and the mandatory role for IL-4Rα in mediating the progression dependent on IL-13 of experimental TB [51].