Evidence map›Paper›PMID 26203637›Full record

ArticleThe Journal of investigative dermatology2015

Integrin αE(CD103) Is Involved in Regulatory T-Cell Function in Allergic Contact Hypersensitivity.

Andrea Braun, Nadin Dewert, Fiona Brunnert, Viktor Schnabel, Jan-Hendrik Hardenberg, Beatrice Richter, Karolin Zachmann, Sascha Cording, Anna Claßen, Richard Brans and 3 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Integrin αCancers · 2021
    Review
  9. T-Cell Adhesion in Healthy and Inflamed Skin.JID innovations : skin science from molecules to population health · 2021
    Review
  10. Article
  11. Contact dermatitis.Nature reviews. Disease primers · 2021
    Review
  12. Tissue-Resident Memory-Like CD8Journal of immunology research · 2021
    Observational
  13. Article
  14. CD103 Promotes the Pro-inflammatory Response of Gastric Resident CD4Frontiers in cellular and infection microbiology · 2020
    Article
  15. Article
  16. Article
  17. Article
  18. CD103Journal of Cancer · 2019
    Article
  19. Article
  20. Article
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

13 authors at 5 institutions in 1 country.

Andrea BraunDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany; Lower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen and University of Osnabrück, Osnabrück, Germany.
Nadin DewertDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.
Fiona BrunnertDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.
Viktor SchnabelDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.
Jan-Hendrik HardenbergDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.
Beatrice RichterDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.
Karolin ZachmannDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany.
Sascha CordingExperimental Rheumatology, German Rheumatism Research Center Berlin and Charité University Medicine Berlin, Campus Mitte, Berlin, Germany.
Anna ClaßenDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany; Lower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen and University of Osnabrück, Osnabrück, Germany.
Richard BransLower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen and University of Osnabrück, Osnabrück, Germany; Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Osnabrück, Germany.
Alf HamannExperimental Rheumatology, German Rheumatism Research Center Berlin and Charité University Medicine Berlin, Campus Mitte, Berlin, Germany.
Jochen HuehnExperimental Rheumatology, German Rheumatism Research Center Berlin and Charité University Medicine Berlin, Campus Mitte, Berlin, Germany; Experimental Immunology, Helmholtz Centre for Infection Research, Braunschweig, Germany.
Michael P SchönDepartment of Dermatology, Venereology, and Allergology, Georg August University, Göttingen, Germany; Lower Saxony Institute of Occupational Dermatology, University Medical Center Göttingen and University of Osnabrück, Osnabrück, Germany. Electronic address: michael.schoen@med.uni-goettingen.de.
University of Göttingen · DEUniversitätsmedizin Göttingen · DECharité - Universitätsmedizin Berlin · DEGerman Rheumatism Research Centre · DEHelmholtz Centre for Infection Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Murine contact hypersensitivity (CHS) is a dendritic cell (DC)-dependent T-cell-mediated inflammation with CD8+ T cells as effectors and CD4+ T cells as regulators (Treg cells) that models human allergic contact dermatitis. The integrin αE(CD103) is expressed by some T-cell and DC subsets and has been implicated in epithelial lymphocyte localization, but its role in immune regulation remains enigmatic. We have identified a function for CD103 in the development of cutaneous allergic immune responses. CHS responses, but not irritant contact dermatitis, were significantly augmented in CD103-deficient mice in hapten-challenged skin. Phenotype and function of skin DCs during sensitization were normal, whereas adoptive transfer experiments revealed that the elevated CHS response in CD103-deficient mice is transferred by primed T cells and is independent of resident cells in recipient mice. While T-cell counts were elevated in challenged skin of CD103-deficient mice, the FoxP3 expression level of CD4+CD25+ Treg cells was significantly reduced, indicating impaired functionality. Indeed, Treg cells from CD103-deficient mice were not able to suppress CHS reactions during the elicitation phase. Further, CD103 on FoxP3+ Treg cells was involved in Treg retention to inflamed skin. These findings indicate an unexpected dichotomous functional role for CD103 on Treg cells by modulating FoxP3 expression.

Indexed as

Adoptive TransferAnimalsAntigens, CDDendritic CellsDermatitis, Allergic ContactForkhead Transcription FactorsHomeodomain ProteinsIntegrin alpha ChainsMiceMice, Inbred BALB CMice, Inbred C57BLSkinT-Lymphocytes, Regulatoryalpha E integrinsAntigens, CDForkhead Transcription FactorsFoxp3 protein, mouseHomeodomain ProteinsIntegrin alpha ChainsRAG-1 protein

Identifiers

PMID26203637
OpenAlexW1442724974

What OpenQuestion holds

Textmetadata
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.