Evidence map›Paper›PMID 35834333›Full record

ArticleThe Journal of clinical investigation2022

Human β-defensin-3 attenuates atopic dermatitis-like inflammation through autophagy activation and the aryl hydrocarbon receptor signaling pathway.

Ge Peng, Saya Tsukamoto, Risa Ikutama, Hai Le Thanh Nguyen, Yoshie Umehara, Juan V Trujillo-Paez, Hainan Yue, Miho Takahashi, Takasuke Ogawa, Ryoma Kishi and 9 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
8.1field-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

42 citing papers in PubMed, 63 citations in OpenAlex.

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  15. Article
  16. Article
  17. Review
  18. Antimicrobial Peptide Signaling in Skin Diseases.JID innovations : skin science from molecules to population health · 2025
    Review
  19. Article
  20. NETs: a new target for autoimmune disease.Frontiers in immunology · 2025
    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

19 authors at 2 institutions in 2 countries.

Ge PengAtopy (Allergy) Research Center and.
Saya TsukamotoAtopy (Allergy) Research Center and.
Risa IkutamaAtopy (Allergy) Research Center and.
Hai Le Thanh NguyenAtopy (Allergy) Research Center and.
Yoshie UmeharaAtopy (Allergy) Research Center and.
Juan V Trujillo-PaezAtopy (Allergy) Research Center and.
Hainan YueAtopy (Allergy) Research Center and.
Miho TakahashiAtopy (Allergy) Research Center and.
Takasuke OgawaDepartment of Dermatology and Allergology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Ryoma KishiJuntendo Itch Research Center, Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Urayasu, Japan.
Mitsutoshi TominagaJuntendo Itch Research Center, Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Urayasu, Japan.
Kenji TakamoriJuntendo Itch Research Center, Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Urayasu, Japan.
Jiro KitauraAtopy (Allergy) Research Center and.
Shun KageyamaDepartment of Physiology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Masaaki KomatsuDepartment of Physiology, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Ko OkumuraAtopy (Allergy) Research Center and.
Hideoki OgawaAtopy (Allergy) Research Center and.
Shigaku IkedaAtopy (Allergy) Research Center and.
François NiyonsabaAtopy (Allergy) Research Center and.
Juntendo University · JPAllergy Associates Research Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human β-defensin-3 (hBD-3) exhibits antimicrobial and immunomodulatory activities; however, its contribution to autophagy regulation remains unclear, and the role of autophagy in the regulation of the epidermal barrier in atopic dermatitis (AD) is poorly understood. Here, keratinocyte autophagy was restrained in the skin lesions of patients with AD and murine models of AD. Interestingly, hBD-3 alleviated the IL-4- and IL-13-mediated impairment of the tight junction (TJ) barrier through keratinocyte autophagy activation, which involved aryl hydrocarbon receptor (AhR) signaling. While autophagy deficiency impaired the epidermal barrier and exacerbated inflammation, hBD-3 attenuated skin inflammation and enhanced the TJ barrier in AD. Importantly, hBD-3-mediated improvement of the TJ barrier was abolished in autophagy-deficient AD mice and in AhR-suppressed AD mice, suggesting a role for hBD-3-mediated autophagy in the regulation of the epidermal barrier and inflammation in AD. Thus, autophagy contributes to the pathogenesis of AD, and hBD-3 could be used for therapeutic purposes.

Indexed as

beta-DefensinsDermatitis, AtopicAnimalsAutophagyHumansInflammationKeratinocytesMiceReceptors, Aryl HydrocarbonSignal Transductionbeta-DefensinsReceptors, Aryl HydrocarbonAutophagyDefensinsDermatologyInflammationTight junctions

Identifiers

PMID35834333
PMCPMC9435650
OpenAlexW4285389910

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.