Evidence map›Paper›PMID 30843878›Full record

ArticleJCI insight2019

Ets1 suppresses atopic dermatitis by suppressing pathogenic T cell responses.

Choong-Gu Lee, Ho-Keun Kwon, Hyeji Kang, Young Kim, Jong Hee Nam, Young Ho Won, Sunhee Park, Taemook Kim, Keunsoo Kang, Dipayan Rudra and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
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  6. The therapeutic potential ofFrontiers in pharmacology · 2025
    Review
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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

13 authors at 7 institutions in 1 country.

Choong-Gu LeeNatural Product Informatics Research Center, Korea Institute of Science and Technology (KIST) Gangneung Institute of Natural Products, Gangneung, South Korea.
Ho-Keun KwonDepartment of Microbiology, College of Medicine, Yonsei University, Seoul, South Korea.
Hyeji KangAcademy of Immunology and Microbiology (AIM), Institute for Basic Science (IBS), Pohang, South Korea.
Young KimDepartment of Oral Pathology, School of Dentistry, Chonnam National University, Gwangju, South Korea.
Jong Hee NamDepartment of Pathology and.
Young Ho WonDepartment of Dermatology, Chonnam National University Medical School, Gwangju, South Korea.
Sunhee ParkAcademy of Immunology and Microbiology (AIM), Institute for Basic Science (IBS), Pohang, South Korea.
Taemook KimDepartment of Microbiology, Dankook University, Cheonan, South Korea.
Keunsoo KangDepartment of Microbiology, Dankook University, Cheonan, South Korea.
Dipayan RudraAcademy of Immunology and Microbiology (AIM), Institute for Basic Science (IBS), Pohang, South Korea.
Chang-Duk JunSchool of Life Sciences, Gwangju Institute of Science and Technology (GIST), Gwangju, South Korea.
Zee Yong ParkSchool of Life Sciences, Gwangju Institute of Science and Technology (GIST), Gwangju, South Korea.
Sin-Hyeog ImAcademy of Immunology and Microbiology (AIM), Institute for Basic Science (IBS), Pohang, South Korea.
Institute for Basic Science · KRDankook University · KRGwangju Institute of Science and Technology · KRPohang University of Science and Technology · KRChonnam National University · KRChonnam National University Hospital · KRYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atopic dermatitis (AD) is a complex inflammatory skin disease mediated by immune cells of both adaptive and innate types. Among them, CD4+ Th cells are one of major players of AD pathogenesis. Although the pathogenic role of Th2 cells has been well characterized, Th17/Th22 cells are also implicated in the pathogenesis of AD. However, the molecular mechanisms underlying pathogenic immune responses in AD remain unclear. We sought to investigate how the defect in the AD susceptibility gene, Ets1, is involved in AD pathogenesis in human and mice and its clinical relevance in disease severity by identifying Ets1 target genes and binding partners. Consistent with the decrease in ETS1 levels in severe AD patients and the experimental AD-like skin inflammation model, T cell-specific Ets1-deficient mice (Ets1ΔdLck) developed severe AD-like symptoms with increased pathogenic Th cell responses. A T cell-intrinsic increase of gp130 expression upon Ets1 deficiency promotes the gp130-mediated IL-6 signaling pathway, thereby leading to the development of severe AD-like symptoms. Functional blocking of gp130 by selective inhibitor SC144 ameliorated the disease pathogenesis by reducing pathogenic Th cell responses. Our results reveal a protective role of Ets1 in restricting pathogenic Th cell responses and suggest a potential therapeutic target for AD treatment.

Indexed as

Adaptive ImmunityAnimalsCD8-Positive T-LymphocytesCytokine Receptor gp130Dermatitis, AtopicDisease Models, AnimalHumansInterleukin-6MiceMice, KnockoutProto-Oncogene Protein c-ets-1SkinTh17 CellsTh2 CellsT-LymphocytesCytokine Receptor gp130ETS1 protein, humanEts1 protein, mouseIL6ST protein, humanIl6st protein, mouseInterleukin-6Proto-Oncogene Protein c-ets-1Adaptive immunityAllergyImmunologyT cells

Identifiers

PMID30843878
PMCPMC6483523
OpenAlexW2919173053

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.