G protein-coupled receptor 83 is dispensable for the development and function of regulatory T cells

Mol Cell Biol. 2007 Dec;27(23):8065-72. doi: 10.1128/MCB.01075-07. Epub 2007 Sep 24.


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 beta-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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • CD8-Positive T-Lymphocytes / cytology
  • CD8-Positive T-Lymphocytes / drug effects
  • Cell Differentiation / drug effects
  • Forkhead Transcription Factors / deficiency
  • Forkhead Transcription Factors / genetics
  • Gene Deletion
  • Gene Targeting
  • Lymphocyte Activation / drug effects
  • Mice
  • Phenotype
  • Receptors, G-Protein-Coupled / deficiency
  • Receptors, G-Protein-Coupled / metabolism*
  • T-Lymphocytes, Helper-Inducer / cytology
  • T-Lymphocytes, Helper-Inducer / drug effects
  • T-Lymphocytes, Regulatory / cytology*
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / metabolism*
  • Transforming Growth Factor beta / pharmacology
  • Up-Regulation / drug effects


  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Gpr83 protein, mouse
  • Receptors, G-Protein-Coupled
  • Transforming Growth Factor beta