Evidence map›Paper›PMID 34867936›Full record

ArticleFrontiers in immunology2021

Essential Role of STAT3 Signaling in Hair Follicle Homeostasis.

Kosuke Miyauchi, Sewon Ki, Masao Ukai, Yoshie Suzuki, Kentaro Inoue, Wataru Suda, Takeshi Matsui, Yoshihiro Ito, Kenya Honda, Haruhiko Koseki and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

8 citing papers in PubMed, 16 citations in OpenAlex.

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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

14 authors at 8 institutions in 2 countries.

Kosuke MiyauchiLaboratory for Cytokine Regulation, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Sewon KiLaboratory for Cytokine Regulation, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Masao UkaiLaboratory for Integrated Cellular Systems, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Yoshie SuzukiLaboratory for Cytokine Regulation, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Kentaro InoueLaboratory for Integrated Cellular Systems, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Wataru SudaLaboratory for Microbiome science, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Takeshi MatsuiLaboratory for Evolutionary Cell Biology of the Skin, School of Bioscience and Biotechnology, Tokyo University of Technology, Hachioji, Japan.
Yoshihiro ItoLaboratory for Gut Homeostasis, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Kenya HondaLaboratory for Gut Homeostasis, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Haruhiko KosekiDisease Biology Group, RIKEN Medical Sciences Innovation Hub Program, Kanagawa, Japan.
Osamu OharaLaboratory for Integrative Genomics, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Reiko J TanakaDepartment of Bioengineering, Imperial College London, London, United Kingdom.
Mariko Okada-HatakeyamaLaboratory for Integrated Cellular Systems, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
Masato KuboLaboratory for Cytokine Regulation, Center for Integrative Medical Science (IMS), RIKEN Yokohama Institute, Yokohama, Japan.
RIKEN Center for Integrative Medical Sciences · JPImperial College London · GBKazusa DNA Research Institute · JPKeio University · JPProtein Research Foundation · JPThe University of Tokyo · JPTokyo University of Technology · JPYokohama City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dominant-negative mutations associated with signal transducer and activator of transcription 3 (STAT3) signaling, which controls epithelial proliferation in various tissues, lead to atopic dermatitis in hyper IgE syndrome. This dermatitis is thought to be attributed to defects in STAT3 signaling in type 17 helper T cell specification. However, the role of STAT3 signaling in skin epithelial cells remains unclear. We found that STAT3 signaling in keratinocytes is required to maintain skin homeostasis by negatively controlling the expression of hair follicle-specific keratin genes. These expression patterns correlated with the onset of dermatitis, which was observed in specific pathogen-free conditions but not in germ-free conditions, suggesting the involvement of Toll-like receptor-mediated inflammatory responses. Thus, our study suggests that STAT3-dependent gene expression in keratinocytes plays a critical role in maintaining the homeostasis of skin, which is constantly exposed to microorganisms.

Indexed as

AnimalsDermatitis, AtopicDisease Models, AnimalFemaleGene Expression RegulationHair FollicleHomeostasisHumansKeratinocytesKeratinsMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutSignal TransductionKeratinsSTAT3 protein, humanStat3 protein, mouseSTAT3 Transcription Factoratopic dermatitisbacteriahair follicle (HF)skinSTAT3 (signal transducer and activator of transcription 3)

Identifiers

PMID34867936
PMCPMC8635990
OpenAlexW3211566568

What OpenQuestion holds

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Registered trials

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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.