MHC class II-dependent basophil-CD4(+) T cell interactions promote T(H)2 cytokine-dependent immunity

J.G. Perrigoue, S.A. Saenz, M.C. Siracusa, E.J. Allenspach, B.C. Taylor, P. Giacomin, M.G. Nair, Y.R. Du, C. Zaph, N. van Rooijen, M.R. Comeau, E.J. Pearce, T.M. Laufer, D. Artis

Research output: Contribution to journalArticleAcademicpeer-review


Dendritic cells can prime naive CD4(+) 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(+) T cell proliferation and interleukin 4 production in vitro, and transfer of basophils augmented the population expansion of helminth-responsive CD4(+) T cells in vivo. Collectively, our studies suggest that major histocompatibility complex class II-dependent interactions between basophils and CD4(+) T cells promote T helper type 2 cytokine responses and immunity to helminth infection
Original languageUndefined/Unknown
Pages (from-to)697-705
JournalNature Immunology
Issue number7
Publication statusPublished - 2009

Cite this