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The Journal of Immunology, 2005, 175: 1694-1705.
Copyright © 2005 by The American Association of Immunologists

Runx3 Regulates Integrin {alpha}E/CD103 and CD4 Expression during Development of CD4–/CD8+ T Cells1

Baerbel Grueter2,*, Michaela Petter3,{ddagger}, Takeshi Egawa||, Kirsten Laule-Kilian4,{ddagger}, Christine J. Aldrian{ddagger}, Andreas Wuerch{ddagger}, Yvonne Ludwig5,*, Hidehiro Fukuyama§, Hedda Wardemann, Ralph Waldschuetz{dagger}, Tarik Möröy{dagger}, Ichiro Taniuchi6,||, Viktor Steimle7,{ddagger}, Dan R. Littman|| and Marc Ehlers8,*,{ddagger},§

* Institute of Molecular Biology (Cancer Research) and {dagger} Institute of Cell Biology (Cancer Research), University of Essen, Medical School, Essen, Germany; {ddagger} Hans Spemann Laboratories, Max Planck Institute for Immunology, Freiburg, Germany; § Laboratory of Molecular Genetics and Immunology and Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10021; and || Howard Hughes Medical Institute and Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016

During thymic T cell development, immature CD4+CD8+ double-positive (DP) thymocytes develop either into CD4+CD8– Th cells or CD4–CD8+ CTLs. Differentially expressed primary factors inducing the fate of these cell types are still poorly described. The transcription factor Runx3/AML-2 Runx, rust dominant factor; AML, acute myeloid leukemia is expressed specifically during the development of CD8 single-positive (SP) thymocytes, where it silences CD4 expression. Deletion of murine Runx3 results in a reduction of CD8 SP T cells and concomitant accumulation of CD4+CD8+ T cells, which cannot down-regulate CD4 expression in the thymus and periphery. In this study we have investigated the role of Runx3 during thymocyte development and CD4 silencing and have identified integrin {alpha}E/CD103 on CD8 SP T cells as a new potential target gene of Runx3. We demonstrate that Runx3 is necessary not only to repress CD4, but also to induce CD103 expression during development of CD8 SP T cells. In addition, transgenic overexpression of Runx3 reduced CD4 expression during development of DP thymocytes, leading to a reduced number of CD4 SP thymocytes and an increased number of CD8 SP thymocytes. This reversal is not caused by redirection of specific MHC class II-restricted cells to the CD8 lineage. Overexpression of Runx3 also up-regulated CD103 expression on a subpopulation of CD4 SP T cells with characteristics of regulatory T cells. Thus, Runx3 is a main regulator of CD4 silencing and CD103 induction and thus contributes to the phenotype of CD8 SP T cells during thymocyte development.




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