| First Author | In TSH | Year | 2017 |
| Journal | Nat Commun | Volume | 8 |
| Issue | 1 | Pages | 2004 |
| PubMed ID | 29222418 | Mgi Jnum | J:257675 |
| Mgi Id | MGI:6112545 | Doi | 10.1038/s41467-017-02225-5 |
| Citation | In TSH, et al. (2017) HEB is required for the specification of fetal IL-17-producing gammadelta T cells. Nat Commun 8(1):2004 |
| abstractText | 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. |
