ArticleMolecular and cellular biology2007
G protein-coupled receptor 83 is dispensable for the development and function of regulatory T cells.
Article in Molecular and cellular biology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- Identification of small molecule ligands for GPR83 that modulate morphine antinociception and reward.Molecular pharmacology · 2026Article
- GPCRs: emerging targets for novel T cell immune checkpoint therapy.Cancer immunology, immunotherapy : CII · 2024Review
- Enkephalin-mediated modulation of basal somatic sensitivity by regulatory T cells in mice.eLife · 2024Article
- Is the Neuropeptide PEN a Ligand of GPR83?International journal of molecular sciences · 2023Article
- Single-Cell RNA Sequencing Reveals Unique Alterations in the Immune Panorama and Treg Subpopulations in Mice during the Late Stages of Echinococcus granulosus Infection.Infection and immunity · 2023Article
- Bone Morphogenetic Proteins Shape TFrontiers in immunology · 2022Review
- Current Insights Into the Role of Neuropeptide Y in Skin Physiology and Pathology.Frontiers in endocrinology · 2022Review
- PEN Receptor GPR83 in Anxiety-Like Behaviors: Differential Regulation in Global vs Amygdalar Knockdown.Frontiers in neuroscience · 2021Article
- The role of the neuropeptide PEN receptor, GPR83, in the reward pathway: Relationship to sex-differences.Neuropharmacology · 2019Article
- Two Proximally Close Priority Candidate Genes for diplopodia-1, an Autosomal Inherited Craniofacial-Limb Syndrome in the Chicken: MRE11 and GPR83.The Journal of heredity · 2019Article
- TGF-β-mediated enhancement of TScience signaling · 2018Article
- Targeting the Recently Deorphanized Receptor GPR83 for the Treatment of Immunological, Neuroendocrine and Neuropsychiatric Disorders.Progress in molecular biology and translational science · 2018Review
- Footprints of Sepsis Framed Within Community Acquired Pneumonia in the Blood Transcriptome.Frontiers in immunology · 2018Article
- Article
- Identification of GPR83 as the receptor for the neuroendocrine peptide PEN.Science signaling · 2016Article
- G-protein coupled receptor 83 (GPR83) signaling determined by constitutive and zinc(II)-induced activity.PloS one · 2013Article
- Downregulation of GPR83 in the hypothalamic preoptic area reduces core body temperature and elevates circulating levels of adiponectin.Metabolism: clinical and experimental · 2012Article
- Inflammation in vivo is modulated by GPR83 isoform-4 but not GPR83 isoform-1 expression in regulatory T cells.Genes and immunity · 2010Article
- Genotype-dependent tumor regression in Marek's disease mediated at the level of tumor immunity.Cancer microenvironment : official journal of the International Cancer Microenvironment Society · 2009Article
- Gpr83 expression is not required for the maintenance of intestinal immune homeostasis and regulation of T-cell-dependent colitis.Immunology · 2008Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.