McFarlane, EMokgethi, TKaye, P.MHurdayal, RBrombacher, FAlexander, JCarter, K.C2024-06-092024-06-092019-08-16McFarlane E, Mokgethi T, Kaye PM, Hurdayal R, Brombacher F, Alexander J and Carter KC. IL-4 mediated resistance of BALB/c mice to visceral leishmaniasis is independent of IL-4Ralpha signaling via T Cells. Frontiers in Immunology. 2019 Aug;10:1957. doi: 10.3389/fimmu.2019.01957https://doi.org/10.3389/fimmu.2019.01957https://www.frontiersin.org/articles/10.3389/fimmu.2019.01957/fullhttps://hdl.handle.net/11288/596382Previous studies infecting global IL-4Rα−/−, IL-4−/−, and IL-13−/−mice on a BALB/c background with the visceralizing parasite Leishmania donovani have shown that the T helper 2 cytokines, IL-4, and IL-13, play influential but not completely overlapping roles in controlling primary infection. Subsequently, using macrophage/neutrophil-specific IL-4Rα deficient BALB/c mice, we demonstrated that macrophage/neutrophil unresponsiveness to IL-4 and IL-13 did not have a detrimental effect during L. donovani infection. Here we expand on these findings and show that CD4+ T cell-(Lckcre), as well as pan T cell-(iLckcre) specific IL-4Rα deficient mice, on a BALB/c background, unlike global IL-4Rα deficient mice, are also not adversely affected in terms of resistance to primary infection with L. donovani. Our analysis suggested only a transient and tissue specific impact on disease course due to lack of IL-4Rα on T cells, limited to a reduced hepatic parasite burden at day 30 post-infection. Consequently, the protective role(s) demonstrated for IL-4 and IL-13 during L. donovani infection are mediated by IL-4Rα-responsive cell(s) other than macrophages, neutrophils and T cells.enAttribution 3.0 United Stateshttp://creativecommons.org/licenses/by/3.0/us/IL-4 mediated resistanceBALB/c MiceArticleFrontiers in Immunology