1. Trypanosoma cruzi trans-sialidase initiates a program independent of the transcription factors RORγt and Ahr that leads to IL-17 production by activated B cells.
- Author
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Bermejo, Daniela A, Jackson, Shaun W, Gorosito-Serran, Melisa, Acosta-Rodriguez, Eva V, Amezcua-Vesely, Maria C, Sather, Blythe D, Singh, Akhilesh K, Khim, Socheath, Mucci, Juan, Liggitt, Denny, Campetella, Oscar, Oukka, Mohamed, Gruppi, Adriana, and Rawlings, David J
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TRYPANOSOMA cruzi ,NEURAMINIDASE ,TRANSCRIPTION factors ,INTERLEUKIN-17 ,B cells ,PHENOTYPES ,LABORATORY mice ,AUTOIMMUNITY - Abstract
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 TH 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 RORγt 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. [ABSTRACT FROM AUTHOR]- Published
- 2013
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