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CCR7 Expression in Developing Thymocytes Is Linked to the CD4 versus CD8 Lineage Decision¹

Xinye Yin^*, Ena Ladi^*, Shiao Wei Chan^*, Ou Li^*, Nigel Killeen, Dietmar J. Kappes and Ellen A. Robey^2,*

^* Department of Molecular and Cell Biology, Division of Immunology, University of California, Berkeley, CA 94720; Department of Microbiology and Immunology, University of California, San Francisco, CA 94143; and Fox Chase Cancer Center, Philadelphia, PA 19111

During thymic development, T cell progenitors undergo positive selection based on the ability of their T cell Ag receptors (TCR) to bind MHC ligands on thymic epithelial cells. Positive selection determines T cell fate, in that thymocytes whose TCR bind MHC class I (MHC-I) develop as CD8-lineage T cells, whereas those that bind MHC class II (MHC-II) develop as CD4 T cells. Positive selection also induces migration from the cortex to the medulla driven by the chemokine receptor CCR7. In this study, we show that CCR7 is up-regulated in a larger proportion of CD4⁺CD8⁺ thymocytes undergoing positive selection on MHC-I compared with MHC-II. Mice bearing a mutation of Th-POK, a key CD4/CD8-lineage regulator, display increased expression of CCR7 among MHC-II-specific CD4⁺CD8⁺ thymocytes. In addition, overexpression of CCR7 results in increased development of CD8 T cells bearing MHC-II-specific TCR. These findings suggest that the timing of CCR7 expression relative to coreceptor down-regulation is regulated by lineage commitment signals.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by Research Grants AI32985 and AI053039 from the National Institutes of Health.

² Address correspondence and reprint requests to Prof. Ellen Robey, University of California, Berkeley, 142 LSA No. 3200, Berkeley, CA 94720. E-mail address: erobey{at}berkeley.edu

³ Abbreviations used in this paper: MHC-II, MHC class II; MHC-I, MHC class I.

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The JI 2007 179: 7191-7192. [Full Text]  

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