Evidence map›Paper›PMID 38566145›Full record

ArticleJournal of translational medicine2024

Double-negative T cells ameliorate psoriasis by selectively inhibiting IL-17A-producing γδ

Yunxiong Wei, Guangyong Sun, Yang Yang, Mingyang Li, Shimeng Zheng, Xiyu Wang, Xinjie Zhong, Zihan Zhang, Xiaotong Han, Haiyan Cheng and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Article
  3. CD4Frontiers in immunology · 2025
    Article
  4. 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

12 authors at 1 institution in 1 country.

Yunxiong Wei *Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Guangyong Sun *Immunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Yang YangImmunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Mingyang LiImmunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Shimeng ZhengMedical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Xiyu WangMedical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Xinjie ZhongImmunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Zihan ZhangImmunology Research Center for Oral and Systemic Health, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Xiaotong HanMedical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China.
Haiyan ChengDepartment of Dermatology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.
Dong ZhangMedical Research Center, Beijing Institute of Respiratory Medicine and Beijing Chao-Yang Hospital, Capital Medical University, Beijing, China. zhangd2010@hotmail.com.ORCID 0000-0002-3404-5173
Xueling MeiDepartment of Dermatology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China. meixueling@ccmu.edu.cn.
Capital Medical University · CN

Funding

Beijing Municipal Administration of Hospitals' Ascent Plan DFL20220103National Natural Science Foundation of China 81970503National Natural Science Foundation of China 82270606Natural Science Foundation of Beijing Municipality 7242041R&D Program of Beijing Municipal Education Commission KZ202210025036Youth Beijing Scholar 035
6 · The paper itself

Abstract

backgroundPsoriasis is a chronic immune-mediated skin condition. Although biologic treatments are effective in controlling psoriasis, some patients do not respond or lose response to these therapies. Thus, new strategies for psoriasis treatment are still urgently needed. Double-negative T cells (DNT) play a significant immunoregulatory role in autoimmune diseases. In this study, we aimed to evaluate the protective effect of DNT in psoriasis and explore the underlying mechanism.

methodsWe conducted a single adoptive transfer of DNT into an imiquimod (IMQ)-induced psoriasis mouse model through tail vein injection. The skin inflammation and IL-17A producing γδ T cells were evaluated.

resultsDNT administration significantly reduced the inflammatory response in mouse skin, characterized by decreased skin folds, scales, and red patches. After DNT treatment, the secretion of IL-17A by RORc

conclusionsDNT could migrate to inflamed skin tissue through CCR5, selectively inhibit IL-17-producing γδ

Indexed as

Interleukin-17PsoriasisAnimalsDisease Models, AnimalHumansImiquimodInflammationMiceNK Cell Lectin-Like Receptor Subfamily KSkinT-LymphocytesImiquimodInterleukin-17NK Cell Lectin-Like Receptor Subfamily KCell therapyDouble Negative T cellsIL-17APsoriasisγδ T cells

Identifiers

PMID38566145
PMCPMC10988838
OpenAlexW4393547646

What OpenQuestion 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 OpenQuestion graph.