The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     
 


Published online November 13, 2009
The Journal of Immunology, 2009, 183, 7244 -7249
Copyright © 2009 by The American Association of Immunologists, Inc.
doi:10.4049/jimmunol.0902313

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jimmunol.0902313v1
183/11/7244    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Related articles in The JI
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Houston, E. G.
Right arrow Articles by Fink, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Houston, E. G., Jr.
Right arrow Articles by Fink, P. J.

MHC Drives TCR Repertoire Shaping, but not Maturation, in Recent Thymic Emigrants1,2

Evan G. Houston, Jr., and Pamela J. Fink3

Department of Immunology, University of Washington, Seattle, Washington 98195

After developing in the thymus, recent thymic emigrants (RTEs) enter the lymphoid periphery and undergo a maturation process as they transition into the mature naive (MN) T cell compartment. This maturation presumably shapes RTEs into a pool of T cells best fit to function robustly in the periphery without causing autoimmunity; however, the mechanism and consequences of this maturation process remain unknown. Using a transgenic mouse system that specifically labels RTEs, we tested the influence of MHC molecules, key drivers of intrathymic T cell selection and naive peripheral T cell homeostasis, in shaping the RTE pool in the lymphoid periphery. We found that the TCRs expressed by RTEs are skewed to longer CDR3 regions compared with those of MN T cells, suggesting that MHC does streamline the TCR repertoire of T cells as they transition from the RTE to the MN T cell stage. This conclusion is borne out in studies in which the representation of individual TCRs was followed as a function of time since thymic egress. Surprisingly, we found that MHC is dispensable for the phenotypic and functional maturation of RTEs.

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 The content is solely the responsibility of the authors and does not necessarily represent the official views of either the National Institutes of Health or the National Cancer Institute.

2 This work was supported by grants from the National Cancer Institute (T32CA0095) (to E.G.H.) and the National Institutes of Health (R01 AI 064318) (to P.J.F.).

3 Address correspondence and reprint requests to Dr. Pamela Fink, University of Washington, I-607 H Health Sciences Building, 1959 NE Pacific Street, Box 357650, Seattle, WA 98195. E-mail address: pfink{at}u.washington.edu

4 Abbreviations used in this paper: RTE, recent thymic emigrant; MN, mature naive; Tg, transgenic; RAG2p-GFP Tg, mice transgenic for GFP under control of the RAG2 promoter; SP, single positive; LIP, lymphopenia-induced proliferation.


Related articles in The JI:

IN THIS ISSUE

The JI 2009 183: 6857-6858. [Full Text]  






HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved.