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We recently generated interleukin-4 (IL-4) receptor alpha-deficient (IL-4Rα−/− ) BALB/c mice and showed evidence for a protective role of IL-13-mediated functions in leishmaniasis. In this study, we investigated the IL-4 expression and T helper 2 (Th2) development inLeishmania major -infected IL-4Rα−/− mice. Here we show that the early burst of IL-4 expression observed inL. major -infected BALB/c mice is independent of IL-4Rα-mediated functions. Subsequently, we confirmed an impaired Th2 development in vitro. Unexpectedly, duringL. major infection, isolated CD4+ IL-4Rα−/− T cells expressed high IL-4- but low gamma interferon (IFN-γ)-specific mRNA, comparable to Th2-polarized BALB/c CD4+ cells and in contrast to Th1-polarized C57BL/6 CD4+ cells. Since antigen-specific restimulated popliteal lymph node cells (PLN) of IL-4Rα−/− mice also responded with high IL-4 but low IFN-γ production, comparable to Th2-polarized cells from wild-type BALB/c mice and in contrast to Th1-polarized C57BL/6 cells, these results suggested an unimpaired Th2 polarization during an established infection withL. major . To further define the observed IL-4 receptor-independent Th2 cell phenotype, we determined an independent Th2 marker, the IL-12 receptor beta-2 (IL-12Rβ2)-specific transcript levels of CD4+ T cells. Confirming Th2 polarization inL. major -infected IL-4Rα−/− mice, comparable IL-12Rβ2 message levels between CD4+ T cells from infected IL-4Rα−/− mice and Th2 cells from BALB/c mice were found, whereas Th1-polarized C57BL/6 cells showed strikingly increased IL-12Rβ2 expression levels. These results indicate that signals mediated by the IL-4Rα are not necessary to induce and sustain an efficient IL-4 expression and Th2 polarization inL. major -infected BALB/c mice and suggest that IL-4Rα-independent mechanisms underlie the default Th2 development inL. major -infected BALB/c mice.

Interleukin-4 Receptor Alpha-Deficient BALB/c Mice Show an Unimpaired T Helper 2 Polarization in Response toLeishmania majorInfection