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Molecular and Cellular Biology, December 2007, p. 8065-8072, Vol. 27, No. 23
0270-7306/07/$08.00+0     doi:10.1128/MCB.01075-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

G Protein-Coupled Receptor 83 Is Dispensable for the Development and Function of Regulatory T Cells

Li-Fan Lu,¹ Marc A. Gavin,^1, Jeffrey P. Rasmussen,¹ and Alexander Y. Rudensky^1,2*

Department of Immunology,¹ Howard Hughes Medical Institute, University of Washington, Seattle, Washington 98195²

Received 18 June 2007/ Returned for modification 20 August 2007/ Accepted 12 September 2007

Global analyses of gene expression in regulatory T (Treg) cells, whose development is critically dependent upon the transcription factor Foxp3, have provided many clues as to the molecular mechanisms these cells employ to control immune responses and establish immune tolerance. Through these studies, G protein-coupled receptor 83 (GPR83) was found to be expressed at high levels in Treg-cell populations. However, its function remained unclear. Recently, it has been suggested that GPR83 is involved in the induction of Foxp3 expression in the peripheral nonregulatory Foxp3^– CD4 T cells. To examine a role for GPR83 in Treg-cell biology, we generated and characterized GPR83-deficient mice. We have shown that GPR83 abolition does not result in measurable pathology or changes in the numbers or function of Foxp3⁺ Treg cells. Furthermore, while in vitro analysis suggested a potential involvement of GPR83 in transforming growth factor ß-dependent Foxp3 induction, there was no difference in the ability of nonregulatory GPR83-deficient and nondeficient Foxp3^– T cells to acquire Foxp3 expression in vivo. Collectively, our results demonstrate that GPR83 is dispensable for Treg-cell development and function.

Published ahead of print on 24 September 2007.

Present address: Amgen Corporation, Seattle, WA.