Evidence map›Paper›PMID 27137868›Full record

ArticleScientific reports2016

Up-regulation of Interferon-inducible protein 16 contributes to psoriasis by modulating chemokine production in keratinocytes.

Tianyu Cao, Shuai Shao, Bing Li, Liang Jin, Jie Lei, Hongjiang Qiao, Gang Wang

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Review
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  6. Article
  7. Mutant p53Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
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  8. Article
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  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Herpes Simplex Virus Type 1 Interactions with the Interferon System.International journal of molecular sciences · 2020
    Review
  16. Review
  17. Serum IFI16 and anti-IFI16 antibodies in psoriatic arthritis.Clinical and experimental immunology · 2020
    Article
  18. Increased frequency of activated CD8Scientific reports · 2019
    Article
  19. Effect of RNA Interference TargetingChinese medical journal · 2018
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Tianyu CaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Shuai ShaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Bing LiDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Liang JinDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Jie LeiDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Hongjiang QiaoDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Gang WangDepartment of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
Xijing Hospital · CNAir Force Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Psoriasis is a common chronic inflammatory skin disease characterized by epidermal hyperplasia and dermal inflammation. Keratinocyte activation is known to play a critical role in psoriasis, but the underlying mechanism remains unclear. Interferon-inducible protein 16 (IFI16), an innate immune system sensor, is reported to affect keratinocyte function. We therefore hypothesized that IFI16 promotes psoriasis by modulating keratinocyte activation. In the present study, we cinfirmed that IFI16 was overexpressed in epidermal keratinocytes of psoriasis patients. In addition, psoriasis-related cytokines, including IFN-γ, TNF-α, IL-17 and IL-22, induced IFI16 up-regulation in keratinocytes via activation of STAT3 signaling. We also observed that IFI16 activated the TBK1-NF-κB signaling, leading to the production of CXCL10 and CCL20. Importantly, knocking down p204, which is reported as the mouse orthologous of human IFI16, inhibited epidermal hyperplasia in mice with imiquimod-induced psoriasiform dermatitis. These findings indicate that IFI16 plays a critical role in the pathogenesis of psoriasis and may be a potential therapeutic target.

Indexed as

AnimalsChemokinesGene Expression RegulationHumansInterferon-gammaInterleukin-17Interleukin-22InterleukinsKeratinocytesMiceNuclear ProteinsPhosphoproteinsPsoriasisSignal TransductionSTAT3 Transcription FactorTumor Necrosis Factor-alphaChemokinesIFI16 protein, humanInterferon-gammaInterleukin-17Interleukin-22InterleukinsNuclear ProteinsPhosphoproteinsSTAT3 Transcription FactorTumor Necrosis Factor-alpha

Identifiers

PMID27137868
PMCPMC4853747
OpenAlexW2346459141

What OpenQuestion holds

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LicenceCC BY
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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.