Evidence map›Paper›PMID 25348153›Full record

ArticleThe Journal of experimental medicine2014

GPR18 is required for a normal CD8αα intestinal intraepithelial lymphocyte compartment.

Xiaoming Wang, Hayakazu Sumida, Jason G Cyster

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

59 citing papers in PubMed, 81 citations in OpenAlex.

  1. Transcriptional regulation and function of GPR18 in macrophage subtype specification.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. GPR55 negatively regulates CD8Journal of molecular histology · 2026
    Article
  4. Article
  5. GPCRs: emerging targets for novel T cell immune checkpoint therapy.Cancer immunology, immunotherapy : CII · 2024
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Xiaoming WangHoward Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143 Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143.
Hayakazu SumidaHoward Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143 Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143.
Jason G CysterHoward Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143 Howard Hughes Medical Institute and Department of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143 Jason.Cyster@ucsf.edu.
Howard Hughes Medical Institute · US

Funding

B LYMPHOCYTE MIGRATION AND HOMEOSTASISR01AI040098 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jason G Cyster · 1997 to 2026
$7.0M
Beta Lymphocyte Migration and HomeostasisR37AI040098 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 2002 to 2011
$3.2M
Howard Hughes Medical InstituteNIAID NIH HHS N01 AI040098
6 · The paper itself

Abstract

Intraepithelial lymphocytes (IELs) play an important role in maintaining the physiology of the small intestine. The majority of mouse IELs express CD8αα and are either γδ or αβ T cells. Although the development and homing of CD8αα IELs have been studied in some detail, the factors controlling their homeostasis and positioning are incompletely understood. Here we demonstrate that G protein-coupled receptor 18 (GPR18) is abundantly expressed in CD8αα IELs and that mice lacking this orphan receptor have reduced numbers of γδT IELs. Mixed bone marrow chimera experiments reveal a markedly reduced contribution of GPR18-deficient cells to the CD8αα IEL compartment and a reduction in the CD8αβ T cell subset. These defects could be rescued by transduction with a GPR18-expressing retrovirus. The GPR18-deficient γδT IELs that remained in mixed chimeras had elevated Thy1, and there were less granzyme B(+) and Vγ7(+) cells, indicating a greater reduction in effector-type cells. Flow cytometric analysis indicated GPR18 deficiency more strongly affected the CD8αα cells in the intraepithelial compared with the adjacent lamina propria compartment. These findings establish a requirement for GPR18 in CD8αα and CD8αβ IELs, and we suggest the receptor has a role in augmenting the accumulation of CD8 T cells in the intraepithelial versus lamina propria compartment.

Indexed as

AnimalsCD8 AntigensCD8-Positive T-LymphocytesEpitheliumFlow CytometryGene ExpressionGranzymesIntestine, SmallLymphocytesMice, Inbred C57BLMice, KnockoutMicroscopy, Fluorescence, MultiphotonReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaReceptors, G-Protein-CoupledReverse Transcriptase Polymerase Chain ReactionCD8 antigen, alpha chainCD8 AntigensGPR18 protein, mouseGranzymesReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaReceptors, G-Protein-CoupledThy-1 Antigens

Identifiers

PMID25348153
PMCPMC4235638
OpenAlexW2166924301

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.