Evidence map›Paper›PMID 39284778›Full record

ArticleJournal of cachexia, sarcopenia and muscle2024

Adenosine A2B receptor activation regulates the balance between T helper 17 cells and regulatory T cells, and inhibits regulatory T cells exhaustion in experimental autoimmune myositis.

Yueyuan Zhou, Limei Kang, Geng Yin, Leiyi Yang, Bo Chen, Binhan Liu, Xiaoyan Zhu, Qibing Xie

Abstract read
In one paragraph

Article in Journal of cachexia, sarcopenia and muscle, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Review
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  6. Genetically Predicted tClinical, cosmetic and investigational dermatology · 2026
    Article
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  11. Apoptotic Vesicles Attenuate Acute Lung InjuryInternational journal of nanomedicine · 2025
    Article
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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

8 authors.

Yueyuan ZhouDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Wuhou District, China.ORCID 0000-0002-3765-2585
Limei KangDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Wuhou District, China.
Geng YinDepartment of General Practice, General Practice Medical Center, West China Hospital, Sichuan University, Chengdu, Wuhou District, China.
Leiyi YangDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Wuhou District, China.
Bo ChenDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Wuhou District, China.
Binhan LiuDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Wuhou District, China.
Xiaoyan ZhuDepartment of Physiology, Naval Medical University, Shanghai, Yangpu District, China.ORCID 0000-0002-7998-6444
Qibing XieDepartment of Rheumatology and Immunology, West China Hospital, Sichuan University, Chengdu, Wuhou District, China.ORCID 0000-0002-6727-1839

Funding

1.3.5 Project for Disciplines of Excellence, West China Hospital, Sichuan Universit ZYJC21024Clinical Research Incubation Project of West China Hospital, Sichuan University 2019HXFH038Clinical Research Incubation Project of West China Hospital, Sichuan University 2021HXFH018Sichuan Science and Technology Program 2021JDRC0045Sichuan Science and Technology Program 2021YFS0164Sichuan Science and Technology Program 24ZDYF0224
6 · The paper itself

Abstract

backgroundIdiopathic inflammatory myopathy (IIM) is a systemic autoimmune disease characterized by skeletal muscle involvement. This study aimed to investigate the role of adenosine receptor signalling pathways in the development of experimental autoimmune myositis (EAM).

methodsAn ecto-5'-nucleotidase (CD73) inhibitor, adenosine receptor agonists, a hypoxia-inducible factor-1α (HIF-1α) inhibitor or a vehicle were administered to control and EAM mice. Murine splenic CD4

resultsPatients with IIM exhibited increased CD73 [dermatomyositis (DM), polymyositis (PM): P < 0.01; immune-mediated necrotizing myopathy (IMNM): P < 0.0001] and adenosine deaminase (ADA) expression (DM: P < 0.001; PM, IMNM: P < 0.0001) in the skeletal muscles, and serum ADA levels [56.7 (95% CI: 53.7, 58.7) vs. 198.8 (95% CI: 186.2, 237.3) ng/μL, P < 0.0001]. Intervention with a CD73 inhibitor exacerbated (P = 0.0461), whereas adenosine receptor agonists (A1: P = 0.0009; A2B: P < 0.0001; A3: P = 0.0001) and the HIF-1α inhibitor (P = 0.0044) alleviated skeletal muscle injury in EAM mice. Elevated expression of programmed cell death protein-1 (PD1: P = 0.0023) and T-cell immunoglobulin and mucin-domain containing-3 (TIM3: P < 0.0001) in skeletal muscles of patients with IIM were correlated with creatine kinase levels (PD1, r = 0.7072, P < 0.0001; TIM3, r = 0.4808, P = 0.0046). PD1

conclusionsThe exhausted T cells may be pathogenic in IIM, and the activation of adenosine A2B receptor signalling pathway can regulate Th17/Treg balance and inhibit Tregs exhaustion, thereby slowing EAM disease progression.

Indexed as

Receptor, Adenosine A2BTh17 CellsT-Lymphocytes, Regulatory5'-NucleotidaseAnimalsAutoimmune DiseasesCross-Sectional StudiesDisease Models, AnimalFemaleHumansMaleMiceMiddle AgedMyositis5'-NucleotidaseReceptor, Adenosine A2BAdenosine A2B receptorExperimental autoimmune myositisHypoxia inducible factor‐1αIdiopathic inflammatory myopathyTregs exhaustion

Identifiers

PMID39284778
PMCPMC11634480

What OpenQuestion holds

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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.