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Journal Article

Eomesodermin Expression in CD4+

MPS-Authors

Lupar,  Ekaterina
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
Center for Chronic Immunodeficiency, University Medical Center Freiburg and University of Freiburg;
Faculty of Biology, University of Freiburg;

Brack,  Maria
Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;
Center for Chronic Immunodeficiency, University Medical Center Freiburg and University of Freiburg;

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Izcue,  A.
Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Lupar, E., Brack, M., Garnier, L., Laffont, S., Rauch, K. S., Schachtrup, K., et al. (2015). Eomesodermin Expression in CD4+. The Journal of Immunology, 195, 4742-4752. doi:doi: 10.4049/jimmunol.1501159.


Cite as: http://hdl.handle.net/someHandle/test/escidoc:902521
Abstract
CD4<sup>+</sup> T cells polarize into effector Th subsets characterized by signature transcription factors and cytokines. Although T-bet drives Th1 responses and represses the alternative Th2, Th17, and Foxp3<sup>+</sup> regulatory T cell fates, the role of the T-bet-related transcription factor eomesodermin (Eomes) in CD4<sup>+</sup> T cells is less well understood. In this study, we analyze the expression and effects of Eomes in mouse CD4<sup>+</sup) T lymphocytes. We find that Eomes is readily expressed in activated CD4<sup>+</sup> Th1 T cells in vivo. Eomes<sup>+</sup> CD4<sup>+</sup> T cells accumulated in old mice, under lymphopenic conditions in a T cell transfer model of colitis, and upon oral Ag administration. However, despite its expression, genetic deletion of Eomes in CD4<sup>+</sup> T cells did not impact on IFN-γ production nor increase Th2 or Th17 responses. In contrast, Eomes deficiency favored the accumulation of Foxp3<sup>+</sup> cells in old mice, after in vivo differentiation of Eomes-deficient naive CD4<sup>+</sup> T cells, and in response to oral Ag in a cell-intrinsic way. Enforced Eomes expression during in vitro regulatory T cell induction also reduced Foxp3 transcription. Likewise, bystander Eomes-deficient CD4<sup>+</sup> T cells were more efficient at protecting from experimental autoimmune encephalitis compared with wild-type CD4<sup>+</sup> T cells. This enhanced capacity of Eomes-deficient CD4<sup>+</sup> T cells to inhibit EAE in trans was associated with an enhanced frequency of Foxp3<sup>+</sup> cells. Our data identify a novel role for Eomes in CD4<sup>+</sup> T cells and indicate that Eomes expression may act by limiting Foxp3 induction, which may contribute to the association of EOMES to susceptibility to multiple sclerosis.