Based on comparative histopathology in IL-13tg and other immunodeficient mice infected with Mtb (data not shown), we favour the interpretation that additional, Mtb replication-independent, effects of IL-4Rα-mediated macrophage activation are critical determinants of the observed characteristic form of central granuloma caseation, that differs from widespread, malorganized tissue necrosis occurring during primary TB in immunodeficient hosts. Here, IL4R is linked to tuberculosis.