Evidence map›Paper›PMID 32415989›Full record

ArticleClinical and experimental immunology2020

Pathological role of excessive DNA as a trigger of keratinocyte proliferation in psoriasis.

Y Luo, T Hara, A Kawashima, Y Ishido, S Suzuki, N Ishii, T Kambara, K Suzuki

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Effects of combined treatment withFood science and biotechnology · 2025
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Clinical & Experimental Immunology: Highlights of 2020.Clinical and experimental immunology · 2021
    Article
  15. Article
  16. Innate Immune-Modulatory Activity ofFrontiers in endocrinology · 2020
    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

8 authors at 4 institutions in 2 countries.

Y LuoDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Tokyo, Japan.ORCID 0000-0003-2792-488X
T HaraLeprosy Research Center, National Institute of Infectious Diseases, Tokyo, Japan.
A KawashimaDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Tokyo, Japan.
Y IshidoDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Tokyo, Japan.
S SuzukiEmergency and Critical Care Medicine, Keio University of School of Medicine, Tokyo, Japan.
N IshiiLeprosy Research Center, National Institute of Infectious Diseases, Tokyo, Japan.
T KambaraDepartment of Dermatology, Yokohama City University Medical Center, Yokohama, Japan.
K SuzukiDepartment of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Tokyo, Japan.
National Institute of Infectious Diseases · JPKeio University · JPTeikyo University · JPYokohama City University Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is characterized by excessive growth and aberrant differentiation of epidermal keratinocytes due to persistent inflammation. However, the underlying mechanism that triggers immune activation in psoriasis is not clear. In this study, we explored excessive DNA as a potential trigger of psoriasis using cultured human keratinocytes and psoriatic skin tissues. We demonstrated that human genomic DNA fragments induced tumour necrosis factor (TNF)-α expression, hyperproliferation and over-expression of heparin-binding epidermal-like growth factor (HB-EGF) and transforming growth factor (TGF)-α, accompanied by defective expression of keratins 1 and 10 in cultured normal human epidermal keratinocytes, which have a similar phenotype to that of keratinocytes in psoriatic skin lesions. In psoriatic lesions, we found high levels of double-stranded (ds)DNA fragments, accompanying keratinocytes expressing Ki-67, HB-EGF and TNF-α. In addition, we showed that 1,25-dihydroxyvitamin D

Indexed as

Cell ProliferationDNA FragmentationCell LineDNAHeparin-binding EGF-like Growth FactorHumansInterleukin-1betaKeratinocytesKi-67 AntigenPsoriasisTransforming Growth Factor alphaTumor Necrosis Factor-alphaDNAHeparin-binding EGF-like Growth FactorIL1B protein, humanInterleukin-1betaKi-67 AntigenTransforming Growth Factor alphaTumor Necrosis Factor-alphaactive vitamin Dgenomic DNAinflammationkeratinocytepsoriasis

Identifiers

PMID32415989
PMCPMC7586253
OpenAlexW3026001769

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.