HEB is required for the specification of fetal IL-17-producing γδ T cells

Tracy S. H. In, Ashton Trotman-Grant, Shawn Fahl, Edward L. Y. Chen, Payam Zarin, Amanda J. Moore, David L. Wiest, Juan Carlos Zúñiga-Pflücker and Michele K. Anderson ()
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Tracy S. H. In: Sunnybrook Research Institute
Ashton Trotman-Grant: Sunnybrook Research Institute
Shawn Fahl: Fox Chase Cancer Center
Edward L. Y. Chen: Sunnybrook Research Institute
Payam Zarin: Sunnybrook Research Institute
Amanda J. Moore: Sunnybrook Research Institute
David L. Wiest: Fox Chase Cancer Center
Juan Carlos Zúñiga-Pflücker: Sunnybrook Research Institute
Michele K. Anderson: Sunnybrook Research Institute

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract 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.

Date: 2017
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DOI: 10.1038/s41467-017-02225-5

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