Evidence map›Paper›PMID 35538596›Full record

ArticleExperimental dermatology2022

Keratinocyte EGF signalling dominates in atopic dermatitis lesions: A comparative RNAseq analysis.

Kate Timms, Hui Guo, Peter Arkwright, Joanne Pennock

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Experimental dermatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. EGF-Induced Macropinocytosis Promotes NAV1-Dependent Internalization of Occludin in Keratinocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  7. Article
  8. 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

4 authors at 2 institutions in 1 country.

Kate TimmsLydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester, UK.ORCID 0000-0003-1764-4964
Hui GuoCenter for Biostatistics, School of Health Sciences, Faculty of Biology Medicine and Health, The University of Manchester, Manchester, UK.
Peter ArkwrightLydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester, UK.
Joanne PennockLydia Becker Institute of Immunology and Inflammation, School of Biological Sciences, Faculty of Biology Medicine and Health, University of Manchester, Manchester, UK.ORCID 0000-0002-8304-2905
University of Manchester · GBManchester Academic Health Science Centre · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) remains a highly heterogenous disorder with a multifactorial aetiology. Whilst keratinocytes are known to play a fundamental role in AD, their contribution to the overall immune landscape in moderate-to-severe AD is still poorly understood. In order to design new therapeutics, further investigation is needed into common disease pathways at the molecular level. We used publicly available whole-tissue RNAseq data (4 studies) and single-cell RNAseq keratinocyte data to identify genes/pathways that are involved in keratinocyte responses in AD and after dupilumab treatment. Transcripts present in both keratinocytes (single-cell) and whole-tissue, referred to as the keratinocyte-enriched lesional skin (KELS) genes, were analysed using functional/pathway analysis. Following statistical testing, 2049 genes (16.8%) were differentially expressed in KELS. Enrichment analyses predicted increases in not only type-1/type-2 immune signalling and chemoattraction, but also in EGF-dominated growth factor signalling. We identified complex crosstalk between keratinocytes and immune cells involving a dominant EGF family signature which converges on keratinocytes with potential immunomodulatory and chemotaxis-promoting consequences. Although keratinocytes express the IL4R, we observed no change in EGF signalling in KELS after three-month treatment with dupilumab, indicating that this pathway is not modulated by dupilumab immunotherapy. EGF family signalling is significantly dysregulated in AD lesions but is not associated with keratinocyte proliferation. EGF signalling pathways in AD require further study.

Indexed as

Dermatitis, AtopicCell ProliferationEpidermal Growth FactorHumansKeratinocytesSignal TransductionSkinEpidermal Growth FactoreczemaimmunopathologyinflammationskinTh2

Identifiers

PMID35538596
PMCPMC9545602
OpenAlexW4280563392

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.