Evidence map›Paper›PMID 31644908›Full record

ArticleCell reports2019

Cutaneous Immune Cell-Microbiota Interactions Are Controlled by Epidermal JunB/AP-1.

Özge Uluçkan, Maria Jiménez, Ben Roediger, Jakob Schnabl, Lucía T Díez-Córdova, Kevin Troulé, Wolfgang Weninger, Erwin F Wagner

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Interaction BetweenCurrent pharmaceutical biotechnology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Adding Fuel to the Fire? The Skin Microbiome in Atopic Dermatitis.The Journal of investigative dermatology · 2024
    Review
  8. Skin microbiota: pathogenic roles and implications in atopic dermatitis.Frontiers in cellular and infection microbiology · 2024
    Review
  9. JunB: a paradigm for Jun family in immune response and cancer.Frontiers in cellular and infection microbiology · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. CARD14eLife · 2020
    Article
  15. 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

8 authors at 4 institutions in 3 countries.

Özge UluçkanCancer Cell Biology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain. Electronic address: ozge.uluckan@novartis.com.
Maria JiménezCancer Cell Biology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Ben RoedigerCentenary Institute, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia.
Jakob SchnablCancer Cell Biology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Lucía T Díez-CórdovaCancer Cell Biology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Kevin TrouléBioinformatics Unit, Structural Biology and Biocomputing Programme, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain.
Wolfgang WeningerCentenary Institute, Faculty of Medicine and Health, The University of Sydney, Camperdown, NSW 2050, Australia; Department of Dermatology, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria.
Erwin F WagnerCancer Cell Biology Program, Spanish National Cancer Research Centre (CNIO), 28029 Madrid, Spain; Department of Dermatology, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria; Department of Dermatology and Department of Laboratory Medicine, Medical University of Vienna, Lazarettgasse 14a, 1090 Vienna, Austria. Electronic address: erwin.wagner@meduniwien.ac.at.
Spanish National Cancer Research Centre · ESCentenary Institute · AUMedical University of Vienna · ATUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a multi-factorial skin disease with a complex inflammatory signature including type 2 and type 17 activation. Although colonization by S. aureus is common in AD, the mechanisms rendering an organism prone to dysbiosis, and the role of IL-17A in the control of S. aureus-induced skin inflammation, are not well understood. Here, we show several pathological aspects of AD, including type 2/type 17 immune responses, elevated IgE, barrier dysfunction, pruritus, and importantly, spontaneous S. aureus colonization in JunB

Indexed as

MicrobiotaAnimalsDermatitis, AtopicEpidermisFemaleHomeodomain ProteinsImmunoglobulin EInterleukin-17MaleMiceMice, Inbred C57BLStaphylococcal InfectionsStaphylococcus aureusTranscription Factor AP-1Transcription FactorsHomeodomain ProteinsImmunoglobulin EInterleukin-17JunB protein, mouseRAG-1 proteinTranscription Factor AP-1Transcription FactorsAP-1atopic dermatitisdysbiosisJunBmicrobiotaskin inflammationtype 2 immunity

Identifiers

PMID31644908
PMCPMC6856727
OpenAlexW2981463123

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.