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Essential role of Mediator subunit Med1 in invariant natural killer T-cell development

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Yue,  Xoajing
Max Planck Society;

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

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Borggrefe,  Tilman
Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society;

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Citation

Yue, X., Izcue, A., & Borggrefe, T. (2011). Essential role of Mediator subunit Med1 in invariant natural killer T-cell development. Proceedings of the National Academy of Sciences U.S.A., 108, 17105-17110.


Cite as: http://hdl.handle.net/11858/00-001M-0000-002B-8DC1-E
Abstract
CD1d-restricted invariant NKT (iNKT) cells are a unique lineage of T lymphocytes that regulate both innate and adaptive immunity. The Mediator complex forms the bridge between transcriptional activators and the general transcription machinery. Med1/TRAP220 (also called DRIP205) is a key component of Mediator that interacts with ligand-bound hormone receptors, such as the vitamin D receptor. Here, we show that T-cell-specific Med1 deficiency results in a specific block in iNKT cell development but the development of conventional αβ T cells remains grossly normal. The defect is cell-intrinsic and depends neither on apoptosis, cell-cycle control, nor on CD1d expression of CD4+CD8+ double-positive thymocytes. Surprisingly, ectopic expression of a Vα14-Jα18 T-cell receptor transgene completely rescues the defect caused by Med1 deficiency. At the molecular level, thymic iNKT cells in Med1-/- animals display reduced levels of IL-2Rβ and T-bet expression and could not complete terminal maturation. Thus, Med1 is essential for a complete intra-thymic development of iNKT cells.