Evidence map›Paper›PMID 32065580›Full record

ArticleeLife2020

Neonatal-derived IL-17 producing dermal γδ T cells are required to prevent spontaneous atopic dermatitis.

Nicholas A Spidale, Nidhi Malhotra, Michela Frascoli, Katelyn Sylvia, Bing Miu, Coral Freeman, Brian D Stadinski, Eric Huseby, Joonsoo Kang

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  5. Aqueous extracts ofFrontiers in pharmacology · 2025
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  6. Review
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  12. Review
  13. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. γδ T cells in tissue physiology and surveillance.Nature reviews. Immunology · 2021
    Review
  19. Skin Resident γδ T Cell Function and Regulation in Wound Repair.International journal of molecular sciences · 2020
    Review
  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

9 authors at 1 institution in 1 country.

Nicholas A SpidaleDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.ORCID 0000-0002-1568-4746
Nidhi MalhotraDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.
Michela FrascoliDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.
Katelyn SylviaDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.
Bing MiuDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.
Coral FreemanDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.
Brian D StadinskiDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.
Eric HusebyDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.
Joonsoo KangDepartment of Pathology, University of Massachusetts Medical School, Worcester, United States.ORCID 0000-0001-8419-7995
University of Massachusetts Chan Medical School · US

Funding

Interplay of Regulatory Innate T Cells and Pathogenic T Clonotypes In DermatitisR01AR071269 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HUSEBY, ERIC S, KANG, JOONSOO · 2017 to 2021
$2.9M
Gene circuits programming IL-17 production in innate lymphocytesR01AI101301 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KANG, JOONSOO · 2013 to 2017
$2.1M
Identification and single cell analysis of embryonic lymphoid progenitors that generate neonatal innate T cellsR01AI147685 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KANG, JOONSOO · 2019 to 2021
$1.5M
NIAID NIH HHS R01 AI101301NIAID NIH HHS R01 AI147685NIAMS NIH HHS R01 AR071269
6 · The paper itself

Abstract

Atopic Dermatitis (AD) is a T cell-mediated chronic skin disease and is associated with altered skin barrier integrity. Infants with mutations in genes involved in tissue barrier fitness are predisposed towards inflammatory diseases, but most do not develop or sustain the diseases, suggesting that there exist regulatory immune mechanisms to prevent aberrant inflammation. The absence of one single murine dermal cell type, the innate neonatal-derived IL-17 producing γδ T (Tγδ17) cells, from birth resulted in spontaneous, highly penetrant AD with many of the major hallmarks of human AD. In Tγδ17 cell-deficient mice, basal keratinocyte transcriptome was altered months in advance of AD induction. Tγδ17 cells respond to skin commensal bacteria and the fulminant disease in their absence was driven by skin commensal bacteria dysbiosis. AD in this model was characterized by highly expanded dermal αβ T clonotypes that produce the type three cytokines, IL-17 and IL-22. These results demonstrate that neonatal Tγδ17 cells are innate skin regulatory T cells that are critical for skin homeostasis, and that IL-17 has dual homeostatic and inflammatory function in the skin.

Indexed as

AnimalsAnimals, NewbornAutoantigensCell DifferentiationDermatitis, AtopicDisease Models, AnimalGene ExpressionInterleukin-17Interleukin-22InterleukinsKeratinocytesLymphocyte ActivationMiceMice, KnockoutReceptors, Antigen, T-Cell, gamma-deltaSkinAutoantigensIl17a protein, mouseInterleukin-17Interleukin-22InterleukinsReceptors, Antigen, T-Cell, gamma-deltaSox13 protein, mouseatopic dermatitisbarrier autoimmunityimmunologyinflammationinterleukin-17mouseskin T cells

Identifiers

PMID32065580
PMCPMC7025821
OpenAlexW3006897160

What OpenQuestion holds

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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 OpenQuestion graph.