Evidence map›Paper›PMID 23695512›Full record

ArticleMucosal immunology2014

Protection against colitis by CD100-dependent modulation of intraepithelial γδ T lymphocyte function.

T F Meehan, D A Witherden, C-H Kim, K Sendaydiego, I Ye, O Garijo, H K Komori, A Kumanogoh, H Kikutani, L Eckmann and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. γδ T cells in colorectal and liver cancer.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Reparative T lymphocytes in organ injury.The Journal of clinical investigation · 2019
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Protective and pro-inflammatory roles of intestinal bacteria.Pathophysiology : the official journal of the International Society for Pathophysiology · 2016
    Review
  18. Article
  19. Review
  20. Review
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

11 authors at 5 institutions in 4 countries.

T F MeehanDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
D A WitherdenDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
C-H KimDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
K SendaydiegoDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
I YeDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
O GarijoDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
H K KomoriDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
A Kumanogoh1] Department of Immunopathology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan [2] World Premier International Immunology Frontier Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
H Kikutani1] Department of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan [2] World Premier International Immunology Frontier Research Center, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan.
L EckmannDepartment of Medicine, University of California, San Diego, California, USA.
W L HavranDepartment of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, California, USA.
Scripps Research Institute · USOsaka International University · JPUniversity of California, San Diego · USWellcome Trust · GBYonsei University · KR

Funding

TL MOLECULES AND GAMMA-DELTA T CELLSP01DK035108 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KAGNOFF, MARTIN FREDERICK · 1986 to 2013
$19.2M
PATHOGENESIS AND IMMUNOLOGY OF DISEASET32AI007244 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 1985 to 2022
$8.8M
EPITHELIAL T CELL SECRETION OF TISSUE SPECIFIC CYTOKINESR01AI036964 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI HAVRAN, WENDY L. · 1996 to 2012
$3.7M
The UCSD Digestive Diseases Research Development CenterR24DK080506 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2008 to 2012
$2.7M
Coreceptors for skin gamma delta T cellsR01AI052257 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI HAVRAN, WENDY L · 2002 to 2006
$1.8M
MOUSE MODELS OF INTESTINAL INFECTION AND INFLAMMATIONK26RR017030 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ECKMANN, LARS · 2004 to 2008
$457k
NCRR NIH HHS K26 RR017030NCRR NIH HHS RR17030NIAID NIH HHS AI36964NIAID NIH HHS AI52257NIAID NIH HHS R01 AI036964NIAID NIH HHS R01 AI052257NIAID NIH HHS T32 AI007244NIAID NIH HHS T32AI07244NIDDK NIH HHS DK35108NIDDK NIH HHS DK80506NIDDK NIH HHS P01 DK035108NIDDK NIH HHS R24 DK080506
6 · The paper itself

Abstract

Intraepithelial γδ T lymphocytes (γδ IEL) have important roles in repair of tissue damage at epithelial sites, such as skin and intestine. Molecules that orchestrate these γδ T-cell functions are not well defined. Recently, interaction of the semaphorin CD100 on skin γδ T cells with plexin B2 on keratinocytes was shown to be important for effective γδ T-cell function in the epidermis, which raised the possibility that CD100 may exert similar functions in the intestinal tract. In this study, we find that CD100 is expressed on all IEL, and plexin B2 is present on all epithelial cells of the mouse colon. Using the dextran sulfate sodium (DSS) mouse model of colitis, disease severity is significantly exacerbated in CD100-deficient (CD100(-/-)) mice, with increased colon ulceration and mucosal infiltration with inflammatory cells. The severe colitis in CD100(-/-) mice is attributable to the failure of the colon epithelium to mount a proliferative response to damage. Unlike wild-type γδ IEL, γδ IEL from CD100(-/-) mice fail to produce keratinocyte growth factor-1 (KGF-1) in response to DSS treatment. Administration of recombinant KGF-1 to CD100(-/-) animals ameliorates disease and reverses colitis susceptibility. These results demonstrate that CD100-mediated signals are critical for effective activation of γδ IEL to produce growth factors, including KGF-1, that are required for healing of the colon epithelium during colitis.

Indexed as

AnimalsAntigens, CDColitisDextran SulfateDisease Models, AnimalFemaleFibroblast Growth Factor 7Gene ExpressionGenetic Predisposition to DiseaseIntestinal MucosaMiceMice, KnockoutNerve Tissue ProteinsReceptors, Antigen, T-Cell, gamma-deltaSemaphorinsT-LymphocytesAntigens, CDCD100 antigenDextran SulfateFibroblast Growth Factor 7Nerve Tissue ProteinsPlxnb2 protein, mouseReceptors, Antigen, T-Cell, gamma-deltaSemaphorins

Identifiers

PMID23695512
PMCPMC3795871
OpenAlexW2063085109

What OpenQuestion holds

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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.