Evidence map›Paper›PMID 40781539›Full record

ArticleCommunications biology2025

Macrophagic Ym1 orchestrates γδT cell-derived IL-17 production and keratinocyte functionality to mediate psoriasis-like skin inflammation.

Wentao Zhang, Fei Li, Yu Wang, Meiyang Fan, Yan Zhao, Yanglong Guan, Yan Zhou, Shemin Lu, Rikard Holmdahl, Liesu Meng and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Wentao Zhang *National-local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Fei Li *Department of Dermatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-2409-9282
Yu WangInstitute of Molecular and Translational Medicine (IMTM), and Department of Biochemistry and Molecular Biology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
Meiyang FanInstitute of Molecular and Translational Medicine (IMTM), and Department of Biochemistry and Molecular Biology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
Yan ZhaoDepartment of Dermatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Yanglong GuanInstitute of Molecular and Translational Medicine (IMTM), and Department of Biochemistry and Molecular Biology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
Yan ZhouDepartment of Dermatology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. yanzhou7798@xjtu.edu.cn.ORCID http://orcid.org/0000-0002-9384-8793
Shemin LuNational-local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Rikard HolmdahlNational-local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.ORCID http://orcid.org/0000-0002-4969-2576
Liesu MengNational-local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. mengliesu@xjtu.edu.cn.ORCID http://orcid.org/0000-0003-1985-050X
Wenhua ZhuNational-local Joint Engineering Research Center of Biodiagnostics and Biotherapy, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China. zhuwenhua@xjtu.edu.cn.ORCID http://orcid.org/0000-0002-2820-2427

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82171724
6 · The paper itself

Abstract

Psoriasis is a chronic inflammatory skin disease, with the IL-17 pathway being a key contributor. Ym1, a positionally cloned inflammation regulatory gene linked to various disorders, has an unclear effect on skin inflammation. In this study, the role of Ym1 was investigated in both mannan and imiquimod-induced psoriasis-like dermatitis models, using Ym1-deficient congenic mice. Natural polymorphism of Ym1 influenced the development of skin inflammation, dependent on macrophages, since adoptive transferring of Ym1-deficient macrophages alleviated disease, whereas recombinant Ym1 worsened it. Particularly, Ym1 congenic mice exhibited decreased IL-17 production in innate immune cells, and depletion of γδT cells mitigated disease and lowered skin IL-17 levels. Additionally, RNA-seq analysis revealed Ym1-regulated keratinization in lesional skin. Recombination Ym1 directly influenced the inflammatory response and proliferation of mouse primary keratinocytes. Collectively, we conclude that Ym1 regulates γδT cell-derived IL-17 production and keratinocyte functionality, and thereby contributes to skin inflammation in mice.

Indexed as

Interleukin-17Intraepithelial LymphocytesKeratinocytesMacrophagesPsoriasisAnimalsbeta-N-AcetylhexosaminidasesDisease Models, AnimalInflammationLectinsMiceMice, Inbred C57BLReceptors, Antigen, T-Cell, gamma-deltaSkinbeta-N-AcetylhexosaminidasesChil3 protein, mouseIl17a protein, mouseInterleukin-17LectinsReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID40781539
PMCPMC12334761

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.