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DC activated via dectin-1 convert Treg into IL-17 producers

Th cells producing IL-17 play a pro-inflammatory role at mucosal surfaces. Treg at the same sites dampen inflammation and prevent immunopathology. Th cells producing IL-17 (Th17) and Treg are thought to be distinct populations defined by expression of the transcription factors ROR-γt and Foxp3, resp...

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Detalles Bibliográficos
Autores principales: Osorio, Fabiola, LeibundGut-Landmann, Salomé, Lochner, Matthias, Lahl, Katharina, Sparwasser, Tim, Eberl, Gérard, Reis e Sousa, Caetano
Formato: Texto
Lenguaje:English
Publicado: WILEY-VCH Verlag 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699423/
https://www.ncbi.nlm.nih.gov/pubmed/19039774
http://dx.doi.org/10.1002/eji.200838950
Descripción
Sumario:Th cells producing IL-17 play a pro-inflammatory role at mucosal surfaces. Treg at the same sites dampen inflammation and prevent immunopathology. Th cells producing IL-17 (Th17) and Treg are thought to be distinct populations defined by expression of the transcription factors ROR-γt and Foxp3, respectively. Here, we show that mouse CD25(+)Foxp3(+) Treg can be converted into a hybrid T-cell population characterized by the expression of Foxp3 and ROR-γt and the production of IL-17. Conversion was observed upon coculture with DC selectively activated via dectin-1, a C-type lectin receptor involved in fungal recognition, and depended on IL-23 produced by DC. Within the Foxp3(+) population, only Foxp3(+)ROR-γt(+) T cells but not Foxp3(+)ROR-γt(−)–T cells become Foxp3(+)IL-17(+) T cells. These results indicate that some Foxp3(+) T cells can produce IL-17 while retaining Foxp3 expression and suggest that Treg could play an unexpected pro-inflammatory role in some settings.