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 Google Scholar Google Scholar Articles by Reinwald, S. Articles by Hansen, W. Search for Related Content PubMed PubMed Citation Articles by Reinwald, S. Articles by Hansen, W.

CD83 Expression in CD4⁺ T Cells Modulates Inflammation and Autoimmunity¹

Simone Reinwald^2,*, Carsten Wiethe^2,, Astrid M. Westendorf^*,¶, Minka Breloer, Michael Probst-Kepper, Bernhard Fleischer, Alexander Steinkasserer, Jan Buer^¶ and Wiebke Hansen^3,¶

^* Department of Mucosal Immunity, Helmholtz Centre for Infection Research, Braunschweig; Department of Dermatology, University of Erlangen, Erlangen; Department of Immunology, Bernhard-Nocht-Institute for Tropical Medicine, Hamburg; Junior Research Group for Xenotransplantation, Department of Visceral and Transplant Surgery, Hannover Medical School, Hannover; and ^¶ Institute of Medical Microbiology, University Hospital, Essen, Germany

The transmembrane protein CD83 has been initially described as a maturation marker for dendritic cells. Moreover, there is increasing evidence that CD83 also regulates B cell function, thymic T cell maturation, and peripheral T cell activation. Herein, we show that CD83 expression confers immunosuppressive function to CD4⁺ T cells. CD83 mRNA is differentially expressed in naturally occurring CD4⁺CD25⁺ regulatory T cells, and upon activation these cells rapidly express large amounts of surface CD83. Transduction of naive CD4⁺CD25^– T cells with CD83 encoding retroviruses induces a regulatory phenotype in vitro, which is accompanied by the induction of Foxp3. Functional analysis of CD83-transduced T cells in vivo demonstrates that these CD83⁺Foxp3⁺ T cells are able to interfere with the effector phase of severe contact hypersensitivity reaction of the skin. Moreover, adoptive transfer of these cells prevents the paralysis associated with experimental autoimmune encephalomyelitis, suppresses proinflammatory cytokines IFN- and IL-17, and increases antiinflammatory IL-10 in recipient mice. Taken together, our data provide the first evidence that CD83 expression can contribute to the immunosuppressive function of CD4⁺ T cells in vivo.

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 Deutsche Forschungsgemeinschaft (Grants STE 432/5-1 and SFB 643 to A.S.) and the ELAN Fonds of the University of Erlangen (to C.W.).

² S.R. and C.W. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Wiebke Hansen, Institute of Medical Microbiology, University Hospital Essen, Virchowstrasse 179, D-45122 Essen, Germany. E-mail address: wiebke.hansen{at}uk-essen.de

⁴ Abbreviations used in this paper: Treg, regulatory T; CD83L, CD83 ligand; CHS, contact hypersensitivity; DC, dendritic cell; DNFB, 2,4-dinitro-1-fluorobenzene; EAE, experimental autoimmune encephalomyelitis; eGFP, enhanced GFP; IRES, internal ribosomal entry site; mCD83, membrane-bound CD83; MOG, myelin oligodendrocyte glycoprotein; RPS9, ribosomal protein S9; sCD83, soluble CD83; tg, transgenic; WT, wild type.