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HEB is required for the specification of fetal IL-17-producing γδ T cells.
In, Tracy S H; Trotman-Grant, Ashton; Fahl, Shawn; Chen, Edward L Y; Zarin, Payam; Moore, Amanda J; Wiest, David L; Zúñiga-Pflücker, Juan Carlos; Anderson, Michele K.
Afiliación
  • In TSH; Sunnybrook Research Institute, 2075 Bayview Avenue, Toronto, ON, M4N 3M5, Canada.
  • Trotman-Grant A; Department of Immunology, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
  • Fahl S; Sunnybrook Research Institute, 2075 Bayview Avenue, Toronto, ON, M4N 3M5, Canada.
  • Chen ELY; Department of Immunology, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
  • Zarin P; Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA, 19111, USA.
  • Moore AJ; Sunnybrook Research Institute, 2075 Bayview Avenue, Toronto, ON, M4N 3M5, Canada.
  • Wiest DL; Department of Immunology, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
  • Zúñiga-Pflücker JC; Sunnybrook Research Institute, 2075 Bayview Avenue, Toronto, ON, M4N 3M5, Canada.
  • Anderson MK; Department of Immunology, University of Toronto, 1 King's College Circle, Toronto, ON, M5S 1A8, Canada.
Nat Commun ; 8(1): 2004, 2017 12 08.
Article en En | MEDLINE | ID: mdl-29222418
IL-17-producing γδ T (γδT17) cells are critical components of the innate immune system. However, the gene networks that control their development are unclear. Here we show that HEB (HeLa E-box binding protein, encoded by Tcf12) is required for the generation of a newly defined subset of fetal-derived CD73- γδT17 cells. HEB is required in immature CD24+CD73- γδ T cells for the expression of Sox4, Sox13, and Rorc, and these genes are repressed by acute expression of the HEB antagonist Id3. HEB-deficiency also affects mature CD73+ γδ T cells, which are defective in RORγt expression and IL-17 production. Additionally, the fetal TCRγ chain repertoire is altered, and peripheral Vγ4 γδ T cells are mostly restricted to the IFNγ-producing phenotype in HEB-deficient mice. Therefore, our work identifies HEB-dependent pathways for the development of CD73+ and CD73- γδT17 cells, and provides mechanistic evidence for control of the γδT17 gene network by HEB.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación del Desarrollo de la Expresión Génica / Desarrollo Fetal / Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico / Linfocitos Intraepiteliales / Inmunidad Innata Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Nat Commun Asunto de la revista: BIOLOGIA / CIENCIA Año: 2017 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Regulación del Desarrollo de la Expresión Génica / Desarrollo Fetal / Factores de Transcripción con Motivo Hélice-Asa-Hélice Básico / Linfocitos Intraepiteliales / Inmunidad Innata Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Nat Commun Asunto de la revista: BIOLOGIA / CIENCIA Año: 2017 Tipo del documento: Article País de afiliación: Canadá Pais de publicación: Reino Unido