Evidence map›Paper›PMID 34157145›Full record

ArticleThe British journal of dermatology2021

Glucocorticoids promote CCL20 expression in keratinocytes.

L Wang, M Yang, X Wang, B Cheng, Q Ju, D Z Eichenfield, B K Sun

Open access · greenAbstract read
In one paragraph

Article in The British journal of dermatology, 2021. 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
2.9field-weighted citation impact, top 9% 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, 20 citations in OpenAlex.

  1. Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Targeting Aquaporin-3 Attenuates Skin Inflammation in Rosacea.International journal of biological sciences · 2023
    Article
  14. Glucocorticoid circadian rhythms in immune function.Seminars in immunopathology · 2022
    Review
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

L WangDepartment of Dermatology, Ren Ji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
M YangState Key Laboratory of Oncogenes and Related Genes, Renji-Med X Clinical Stem Cell Research Center, Ren Ji Hospital, Shanghai, 200127, China.
X WangDepartment of Dermatology, Ruijin Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
B ChengDepartment of Dermatology, University of California San Diego, La Jolla, CA, 92093, USA.
Q JuDepartment of Dermatology, Ren Ji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, 200127, China.
D Z EichenfieldDepartment of Dermatology, University of California San Diego, La Jolla, CA, 92093, USA.
B K SunDepartment of Dermatology, University of California San Diego, La Jolla, CA, 92093, USA.ORCID 0000-0002-0740-0125
University of California San Diego · USRenji Hospital · CNRuijin Hospital · CNState Key Laboratory of Oncogene and Related Genes · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlucocorticoids (GCs) are generally envisioned as immunosuppressive, but in conditions such as rosacea and perioral dermatitis they can lead to increased skin inflammation. In lung epithelia, GCs promote expression of the proinflammatory cytokine CCL20, which contributes to steroid-resistant asthma. In the skin, CCL20 stimulates inflammation by recruiting T helper 17 T lymphocytes and dendritic cells, and is elevated in papulopustular rosacea.

objectivesTo understand if, and how, GCs affect CCL20 expression in human keratinocytes. CCL20 expression was assessed by quantitative reverse transcriptase polymerase chain reaction and enzyme-linked immunosorbent assay.

methodsSelective inhibition of candidate genes and signalling pathways was performed using RNA interference and chemical inhibitors. The binding of activated GC receptor to genomic DNA was determined by chromatin immunoprecipitation, and enhancer activity of genomic sequences was measured with a reporter assay.

resultsWe found that GC treatment increased CCL20 expression in human keratinocytes and murine skin, both in the undisturbed state and with tumour necrosis factor-α stimulation. GC repressed proinflammatory signalling pathways, including nuclear factor kappa B and p38/mitogen-activated protein kinase, but these inhibitory effects were opposed by the direct binding of activated GC receptor to the CCL20 enhancer, promoting CCL20 expression.

conclusionsViewed together, these findings demonstrate a mechanism by which GCs induce expression of CCL20 in keratinocytes, which may contribute to the inflammation seen in steroid-exacerbated skin conditions.

Indexed as

GlucocorticoidsKeratinocytesAnimalsChemokine CCL20HumansMiceNF-kappa Bp38 Mitogen-Activated Protein KinasesSignal TransductionCCL20 protein, humanChemokine CCL20GlucocorticoidsNF-kappa Bp38 Mitogen-Activated Protein Kinases

Identifiers

PMID34157145
PMCPMC9290737
OpenAlexW3192581492

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.