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G Protein-Coupled Receptor 83 Overexpression in Naive CD4⁺CD25^– T Cells Leads to the Induction of Foxp3⁺ Regulatory T Cells In Vivo¹

Wiebke Hansen^*, Karin Loser, Astrid M. Westendorf^*, Dunja Bruder^*, Susanne Pfoertner^*, Christiane Siewert, Jochen Huehn, Stefan Beissert and Jan Buer^2,*,

^* Department of Mucosal Immunity, German Research Centre for Biotechnology, Braunschweig, Germany; Department of Dermatology, University of Münster, Münster, Germany; Experimental Rheumatology, Charité University Medicine Berlin, Berlin, Germany; and Institute of Medical Microbiology, Hannover Medical School, Hannover, Germany

Foxp3 functions as a lineage specification factor for the development of naturally occurring thymus-derived CD4⁺CD25⁺ regulatory T (Treg) cells. Recent evidence suggests that naive Foxp3^–CD4⁺CD25^– T cells can be converted in the periphery into Foxp3⁺ Treg cells. In this study, we have identified the G protein-coupled receptor (GPR)83 to be selectively up-regulated by CD4⁺CD25⁺ Treg cells of both murine and human origin in contrast to naive CD4⁺CD25^– or recently activated T cells. Furthermore, GPR83 was induced upon overexpression of Foxp3 in naive CD4⁺CD25^– T cells. Transduction of naive CD4⁺CD25^– T cells with GPR83-encoding retroviruses did not confer in vitro suppressive activity. Nevertheless, GPR83-transduced T cells were able to inhibit the effector phase of a severe contact hypersensitivity reaction of the skin, indicating that GPR83 itself or GPR83-mediated signals conferred suppressive activity to conventional CD4⁺ T cells in vivo. Most strikingly, this in vivo acquisition of suppressive activity was associated with the induction of Foxp3 expression in GPR83-transduced CD4⁺ T cells under inflammatory conditions. Our results suggest that GPR83 might be critically involved in the peripheral generation of Foxp3⁺ Treg cells in vivo.

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