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In TS, Trotman-Grant A, Fahl S, Chen EL, Zarin P, Moore AJ, Wiest DL, Zuniga-Pflucker JC, Anderson MK
HEB is required for the specification of fetal IL-17-producing gammadelta T cells
Nat Commun (2017) 8:2004.
Abstract
IL-17-producing gammadelta T (gammadeltaT17) 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(-) gammadeltaT17 cells. HEB is required in immature CD24(+)CD73(-) gammadelta 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(+) gammadelta T cells, which are defective in RORgammat expression and IL-17 production. Additionally, the fetal TCRgamma chain repertoire is altered, and peripheral Vgamma4 gammadelta T cells are mostly restricted to the IFNgamma-producing phenotype in HEB-deficient mice. Therefore, our work identifies HEB-dependent pathways for the development of CD73(+) and CD73(-) gammadeltaT17 cells, and provides mechanistic evidence for control of the gammadeltaT17 gene network by HEB.
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Publication Date: 2017-12-08.
PMCID: PMC5722817
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Last updated on Monday, August 05, 2019