Evidence map›Paper›PMID 34197663›Full record

ArticleExperimental dermatology2021

Interferon-γ downregulates tight junction function, which is rescued by interleukin-17A.

Yukiko Mizutani, Nao Takagi, Haruna Nagata, Shintaro Inoue

Open access · hybridAbstract read
In one paragraph

Article in Experimental dermatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  3. Fungal Reactive Oxygen Species Secreted byJournal of fungi (Basel, Switzerland) · 2026
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  15. Frontiers in immunology · 2023
    Review
  16. Review
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  18. Skin barrier defects in atopic dermatitis: From old idea to new opportunity.Allergology international : official journal of the Japanese Society of Allergology · 2022
    Review
  19. Article
  20. Review
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 1 institution in 1 country.

Yukiko MizutaniDepartment of Cosmetic Health Science, Gifu Pharmaceutical University, Gifu, Japan.ORCID 0000-0002-1018-9156
Nao TakagiDepartment of Cosmetic Health Science, Gifu Pharmaceutical University, Gifu, Japan.
Haruna NagataDepartment of Cosmetic Health Science, Gifu Pharmaceutical University, Gifu, Japan.
Shintaro InoueDepartment of Cosmetic Health Science, Gifu Pharmaceutical University, Gifu, Japan.ORCID 0000-0002-4996-5693
Gifu Pharmaceutical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although atopic dermatitis (AD) has been reported to be a typical type 2 immune response disease, it is also an inflammatory skin disease that involves cytokines, such as Th1, Th17 and Th22. However, little is known about the mechanism by which the candidate cytokines, alone or in combination, are involved in AD pathology. Differences in cytokine balance, which contribute to the complexity of AD pathology, may influence the stratum corneum barrier function through tight junction (TJ) functional stability and contribute to disease severity. To confirm the regulatory mechanism of TJ protein expression in AD, we investigated the Th1 and Th17 pathways, which are the initiation factors of chronic AD pathology. We examined the effects of these cytokines on TJ protein expression in normal human epidermal keratinocytes in vitro, and also examined their function in a human skin equivalent model. We observed a time- and dose-dependent inhibitory effect of IFN-γ on claudin-1 expression via the IFN-γ receptor/JAK/STAT signalling pathway. IFN-γ impaired TJ function in a human skin equivalent model. Moreover, we investigated co-stimulation with IL-17A, which is highly expressed in AD skin lesions and found that IL-17A restores IFN-γ-induced TJ dysfunction. This restoration of TJ function was mediated by atypical protein kinase C zeta activation without recovery of TJ protein expression. These results are informative for personalized AD treatment via systemic therapies using anti-cytokine antibodies and/or JAK inhibitors.

Indexed as

Claudin-1CytokinesDermatitis, AtopicDown-RegulationHumansInterferon-gammaInterleukin-17Tight JunctionsClaudin-1CytokinesIL17A protein, humanInterferon-gammaInterleukin-17atopic dermatitisatypical protein kinase zetacytokinesJanus kinasekeratinocytes

Identifiers

PMID34197663
PMCPMC9290956
OpenAlexW3173177092

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.