MHC class II-dependent basophil-[CD4.sup.+] T cell interactions promote [T.sub.H]2 cytokine-dependent immunity

Dendritic cells can prime naive [CD4.sup.+] T cells; however, here we demonstrate that dendritic cell-mediated priming was insufficient for the development of T helper type 2 cell-dependent immunity. We identify basophils as a dominant cell population that coexpressed major histocompatibility complex class II and interleukin 4 message after helminth infection. Basophilia was promoted by thymic stromal lymphopoietin, and depletion of basophils impaired immunity to helminth infection. Basophils promoted antigen-specific [CD4.sup.+] T cell proliferation and interleukin 4 production in vitro, and transfer of basophils augmented the population expansion of helminth-responsive [CD4.sup.+] T cells in vivo. Collectively, our studies suggest that major histocompatibility complex class II-dependent interactions between basophils and [CD4.sup.+] T cells promote T helper type 2 cytokine responses and immunity to helminth infection.