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IL-4 Mediated Resistance of BALB/c Mice to Visceral Leishmaniasis Is Independent of IL-4Rα Signaling via T Cells

Previous 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. S...

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Detalles Bibliográficos
Autores principales: McFarlane, Emma, Mokgethi, Thabang, Kaye, Paul M., Hurdayal, Ramona, Brombacher, Frank, Alexander, James, Carter, Katharine C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6707061/
https://www.ncbi.nlm.nih.gov/pubmed/31475014
http://dx.doi.org/10.3389/fimmu.2019.01957
Descripción
Sumario:Previous 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-(Lck(cre)), as well as pan T cell-(iLck(cre)) 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.