HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zehn, D. Articles by Fink, P. J. Search for Related Content PubMed PubMed Citation Articles by Zehn, D. Articles by Fink, P. J.

Cutting Edge: TCR Revision Affects Predominantly Foxp3^– Cells and Skews Them toward the Th17 Lineage¹

Dietmar Zehn^*,, Michael J. Bevan^*, and Pamela J. Fink^2,*

^* Department of Immunology and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195

CD4⁺ T cells respond to peripheral endogenous superantigen stimulation by undergoing deletion or TCR revision. The latter involves RAG re-expression, TCR gene rearrangement, and expression of a novel TCR. TCR-revised T cells are functional and express a diverse TCR repertoire. Because TCR revision harbors the potential to create self-reactivity, it is important to explore whether T cells known to be self-reactive (regulatory T cells) or those involved in autoimmunity (Th17 cells) arise from TCR revision. Interestingly, we observed that Foxp3⁺ cells are excluded from revising their TCR and that only a small fraction of postrevision cells expresses Foxp3. In contrast, Th17 cells are 20 times more frequent among revised than among C57BL/6 CD4⁺ T cells, indicating that postrevision cells are biased toward the Th17 lineage. The link between Th17 differentiation and TCR revision might be highly relevant to the role of Th17 cells in promoting autoimmunity.

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 the Howard Hughes Medical Institute, National Institutes of Health Grants AI19335 (to M.J.B.) and AG13078 (to P.J.F.), and a fellowship from the German Academic Exchange Service (DAAD) (to D.Z.).

² Address correspondence and reprint requests to Dr. Pamela J. Fink, Department of Immunology, University of Washington, Box 357650, Seattle, WA 98195. E-mail address: pfink{at}u.washington.edu

³ Abbreviations used in this paper: Treg, regulatory T cell; B6, C57BL/6; Mtv, mammary tumor virus; Tg, transgenic; V5, V5 TCR -chain.

This article has been cited by other articles:

				M. Mahic, S. Yaqub, T. Bryn, K. Henjum, D. M. Eide, K. M. Torgersen, E. M. Aandahl, and K. Tasken Differentiation of naive CD4+ T cells into CD4+CD25+FOXP3+ regulatory T cells by continuous antigen stimulation J. Leukoc. Biol., May 1, 2008; 83(5): 1111 - 1117. [Abstract] [Full Text] [PDF]