期刊
NATURE IMMUNOLOGY
卷 14, 期 5, 页码 514-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2569
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资金
- US National Institutes of Health [HD037091, HL075453, AI084457, AI071163, AI 075589, 5T32AR007108, K12HD043376]
- Rheumatology Research Foundation
- Consejo Nacional de Investigaciones Cientificas y Tecnicas
- Agencia Nacional de Promocion Cientifica y Tecnologica (Fondo para la Investigacion Cientifica y Tecnologica)
- Secretaria de Ciencia y Tecnologia de la Universidad Nacional de Cordoba
Here we identified B cells as a major source of rapid, innate-like production of interleukin 17 (IL-17) in vivo in response to infection with Trypanosoma cruzi. IL-17(+) B cells had a plasmablast phenotype, outnumbered cells of the T(H)17 subset of helper T cells and were required for an optimal response to this pathogen. With both mouse and human primary B cells, we found that exposure to parasite-derived trans-sialidase in vitro was sufficient to trigger modification of the cell-surface mucin CD45, which led to signaling dependent on the kinase Btk and production of IL-17A or IL-17F via a transcriptional program independent of the transcription factors ROR gamma t and Ahr. Our combined data suggest that the generation of IL-17(+) B cells may be a previously unappreciated feature of innate immune responses required for pathogen control or IL-17-mediated autoimmunity.
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