Evidence map›Paper›PMID 31438472›Full record

ArticleInternational journal of molecular sciences2019

Antagonistic Effects of IL-4 on IL-17A-Mediated Enhancement of Epidermal Tight Junction Function.

Matthew G Brewer, Takeshi Yoshida, Fiona I Kuo, Sade Fridy, Lisa A Beck, Anna De Benedetto

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 33 citations in OpenAlex.

  1. Journal of microbiology and biotechnology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Type 2 Inflammation Contributes to Skin Barrier Dysfunction in Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2022
    Review
  10. The Fate of Epidermal Tight Junctions in theInternational journal of molecular sciences · 2022
    Article
  11. Article
  12. Article
  13. Skin barrier defects in atopic dermatitis: From old idea to new opportunity.Allergology international : official journal of the Japanese Society of Allergology · 2022
    Review
  14. Article
  15. Review
  16. Article
  17. 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

6 authors at 1 institution in 1 country.

Matthew G BrewerDepartment of Dermatology, University of Rochester Medical Center, Rochester, NY 14642, USA.ORCID 0000-0001-7631-5234
Takeshi YoshidaDepartment of Dermatology, University of Rochester Medical Center, Rochester, NY 14642, USA.ORCID 0000-0003-0133-5067
Fiona I KuoDepartment of Dermatology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Sade FridyDepartment of Dermatology, University of Rochester Medical Center, Rochester, NY 14642, USA.
Lisa A BeckDepartment of Dermatology, University of Rochester Medical Center, Rochester, NY 14642, USA.ORCID 0000-0002-8452-667X
Anna De BenedettoDepartment of Dermatology, University of Rochester Medical Center, Rochester, NY 14642, USA. adebenedetto@ufl.edu.
University of Rochester Medical Center · US

Funding

The Role of Keratinocytes as Independent ThermosensorsP30AR057216 · NIAMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI PEREZ WHITE, BETHANY E · 2009 to 2018
$6.0M
Dermatology Foundation research grantNational Eczema Association Research grantNIAMS NIH HHS P30 AR057216
6 · The paper itself

Abstract

Atopic dermatitis (AD) is the most common chronic and relapsing inflammatory skin disease. AD is typically characterized by skewed T helper (Th) 2 inflammation, yet other inflammatory profiles (Th1, Th17, Th22) have been observed in human patients. How cytokines from these different Th subsets impact barrier function in this disease is not well understood. As such, we investigated the impact of the canonical Th17 cytokine, IL-17A, on barrier function and protein composition in primary human keratinocytes and human skin explants. These studies demonstrated that IL-17A enhanced tight junction formation and function in both systems, with a dependence on STAT3 signaling. Importantly, the Th2 cytokine, IL-4 inhibited the barrier-enhancing effect of IL-17A treatment. These observations propose that IL-17A helps to restore skin barrier function, but this action is antagonized by Th2 cytokines. This suggests that restoration of IL-17/IL-4 ratio in the skin of AD patients may improve barrier function and in so doing improve disease severity.

Indexed as

Cells, CulturedClaudin-4Dermatitis, AtopicEpidermisHumansInterleukin-17Interleukin-4In Vitro TechniquesKeratinocytesSkinSTAT3 Transcription FactorTight JunctionsClaudin-4Interleukin-17Interleukin-4STAT3 Transcription Factoratopic dermatitisclaudincytokinesSTAT3tight junctions

Identifiers

PMID31438472
PMCPMC6747459
OpenAlexW2969707257

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.