Artículo
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
Bermejo, Daniela Andrea
; Jackson, Shaun W.; Gorosito Serran, Melisa
; Acosta Rodriguez, Eva Virginia
; Amezcua Vesely, Maria Carolina
; Sather, Blythe D.; Singh, Akhilesh K.; Khim, Socheath; Mucci, Juan Sebastián
; Liggitt, Denny; Campetella, Oscar Eduardo
; Oukka, Mohamed; Gruppi, Adriana
; Rawlings, David J.
Fecha de publicación:
04/2013
Editorial:
Nature Publishing Group
Revista:
Nature Immunology (print)
ISSN:
1529-2908
Idioma:
Inglés
Tipo de recurso:
Artículo publicado
Clasificación temática:
Resumen
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 TH17 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.
Palabras clave:
B Cells
,
Interleukin 17
,
Rorgt
,
Trypanosoma
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Articulos(CIBICI)
Articulos de CENTRO DE INV.EN BIOQUI.CLINICA E INMUNOLOGIA
Articulos de CENTRO DE INV.EN BIOQUI.CLINICA E INMUNOLOGIA
Citación
Bermejo, Daniela Andrea; Jackson, Shaun W.; Gorosito Serran, Melisa; Acosta Rodriguez, Eva Virginia; Amezcua Vesely, Maria Carolina; et al.; 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; Nature Publishing Group; Nature Immunology (print); 14; 4-2013; 514-522
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