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Cutting Edge: The Chemokine Receptor CXCR3 Retains Invariant NK T Cells in the Thymus¹

Michael B. Drennan^2,*, Ann-Sophie Franki^2,, Pieter Dewint^2,*, Katrien Van Beneden^*, Sylvie Seeuws^*, Serge A. van de Pavert, Emma C. Reilly, Gust Verbruggen^*, Thomas E. Lane^¶, Reina E. Mebius, Dieter Deforce and Dirk Elewaut^3,*

^* Laboratory for Molecular Immunology and Inflammation, Department of Rheumatology, Ghent University Hospital and Laboratory for Pharmaceutical Biotechnology, Faculty of Pharmaceutical Sciences, Ghent University, Ghent, Belgium; Department of Molecular Cell Biology and Immunology, Vrije Universiteit University Medical Center, Amsterdam, The Netherlands; Department of Molecular Microbiology and Immunology, Division of Biology and Medicine, Brown University, Providence, RI 02912; and ^¶ Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697

The current model used to define T cell export from the thymus suggests that emigrating lymphocytes seed the peripheral organs as functionally mature cells. This model holds true for the majority of T cells exported from the thymus with the exception of invariant NK T (iNKT) cells. iNKT cells undergo lineage expansion after positive selection and acquire NK receptor expression once fully mature; yet, the majority of mature iNKT cells are retained in the thymus by an as of yet unidentified mechanism. In this study we demonstrate that mature iNKT cells are retained in the thymus by the chemokine receptor CXCR3. We propose that the expression of CXCR3 ligands in the thymic medullary epithelium promotes the chemotactic retention of mature iNKT thymocytes and prevents leakage of iNKT cells into the peripheral circulation.

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 study was supported by grants from the Fund for Scientific Research-Flanders (Belgium) and from the Research-Fund of Ghent University, Ghent, Belgium. A.-S.F. and K.V.B. were postdoctoral fellows supported by the Fund for Scientific Research-Flanders (Belgium). M.B.D. is a postdoctoral fellow supported by the Research Fund of Ghent University. P.D. was a research assistant of the Fund for Scientific Research-Flanders (Belgium).

² M.B.D., A.-S.F., and P.D. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Dirk Elewaut, Ghent University Hospital, Laboratory for Molecular Immunology and Inflammation, Department of Rheumatology, 185 De Pintelaan, B-9000 Ghent. E-mail address: Dirk.Elewaut{at}UGent.be

⁴ Abbreviations used in this paper: iNKT, invariant NK T (cell); RTE, recent thymic emigrant; PB, peripheral blood.

⁵ The online version of this article contains supplemental material.