Journal
NATURE IMMUNOLOGY
Volume 10, Issue 7, Pages 697-U45Publisher
NATURE PORTFOLIO
DOI: 10.1038/ni.1740
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Funding
- NCI NIH HHS [T32 CA09140-30] Funding Source: Medline
- NIAID NIH HHS [R01 AI074878-02, AI61570, R01 AI074878, AI53825, R56 AI032573, T32 AI007532, AI074878, T32 AI007532-08, R01 AI053825, R01 AI061570, R01 AI032573, AI32573, R01 AI061570-05] Funding Source: Medline
- NIDDK NIH HHS [P30 DK050306, DK50306] Funding Source: Medline
- NIGMS NIH HHS [F31 GM082187] Funding Source: Medline
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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.
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