Evidence map›Paper›PMID 30446754›Full record

ReviewNature immunology2018

The epithelial immune microenvironment (EIME) in atopic dermatitis and psoriasis.

Teruki Dainichi, Akihiko Kitoh, Atsushi Otsuka, Saeko Nakajima, Takashi Nomura, Daniel H Kaplan, Kenji Kabashima

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 1 pooled it
30.9field-weighted citation impact, top 1% 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

196 citing papers in PubMed, 1 synthesis or guideline pooled it, 374 citations in OpenAlex.

  1. Pooled it
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  5. Observational
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  11. CD73Nature communications · 2026
    Article
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  13. Keratinocytes: pleiotropic orchestrators of cutaneous immunity and Inflammation - Emerging therapeutic paradigms in dermatological pathologies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  14. Inflammatory niches as spatial drivers of disease mechanisms and targets for personalized treatment.Journal of the European Academy of Dermatology and Venereology : JEADV · 2026
    Review
  15. Article
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  18. Article
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136 more citing papers are in PubMed but not listed here.

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

7 authors at 3 institutions in 3 countries.

Teruki DainichiDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. dainichi@kuhp.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0002-9497-0029
Akihiko KitohDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Atsushi OtsukaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Saeko NakajimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takashi NomuraDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Daniel H KaplanDepartment of Dermatology and Department of Immunology, Cutaneous Biology Research Core, University of Pittsburgh, Pittsburgh, PA, USA.
Kenji KabashimaDepartment of Dermatology, Kyoto University Graduate School of Medicine, Kyoto, Japan. kaba@kuhp.kyoto-u.ac.jp.ORCID http://orcid.org/0000-0002-0773-0554
Kyoto University · JPAgency for Science, Technology and Research · SGUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The skin provides both a physical barrier and an immunologic barrier to external threats. The protective machinery of the skin has evolved to provide situation-specific responses to eliminate pathogens and to provide protection against physical dangers. Dysregulation of this machinery can give rise to the initiation and propagation of inflammatory loops in the epithelial microenvironment that result in inflammatory skin diseases in susceptible people. A defective barrier and microbial dysbiosis drive an interleukin 4 (IL-4) loop that underlies atopic dermatitis, while in psoriasis, disordered keratinocyte signaling and predisposition to type 17 responses drive a pathogenic IL-17 loop. Here we discuss the pathogenesis of atopic dermatitis and psoriasis in terms of the epithelial immune microenvironment-the microbiota, keratinocytes and sensory nerves-and the resulting inflammatory loops.

Indexed as

AnimalsDermatitis, AtopicDysbiosisEpitheliumHumansPsoriasisSkin

Identifiers

PMID30446754
OpenAlexW2899740373

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.