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      Down-regulation of the orphan nuclear receptor ROR gamma t is essential for T lymphocyte maturation.

      The Journal of Immunology Author Choice
      Animals, Antigens, CD95, metabolism, Cell Differentiation, genetics, immunology, Crosses, Genetic, Down-Regulation, Fas Ligand Protein, Gene Expression Regulation, Immunosuppressive Agents, pharmacology, Interleukin-2, antagonists & inhibitors, biosynthesis, Ligands, Lymphocyte Activation, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Transgenic, Nuclear Receptor Subfamily 1, Group F, Member 3, Proto-Oncogene Proteins c-rel, Receptors, Antigen, T-Cell, Receptors, Cytoplasmic and Nuclear, physiology, Receptors, Retinoic Acid, Receptors, Thyroid Hormone, T-Lymphocyte Subsets, cytology, Thymus Gland, Transgenes, Up-Regulation

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          Abstract

          Thymocyte development is a tightly regulated process. CD4+CD8+ double-positive (DP) immature thymocytes exhibit distinct phenotypic features from mature T cells; they express only 10% of surface TCR that are found on mature T cells and do not proliferate and produce IL-2 in response to stimulation. In this report we show that transgenic expression of the orphan nuclear receptor ROR gamma t in mature T cells down-regulates their surface TCR expression. The ROR gamma t transgene inhibits IL-2 production by mature T cells, and this inhibition may be partially due to the inhibitory effect of ROR gamma t on c-Rel transcription. Furthermore, ectopic expression of ROR gamma t inhibits the proliferation of mature and immature T cells. These results, together with its predominant expression in DP thymocytes, suggest that ROR gamma t controls these distinct phenotypic features of DP thymocytes. Our data suggest that down-regulation of ROR gamma t expression in thymocytes is essential for their maturation.

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