Evidence map›Paper›PMID 42260739›Full record

ArticleJournal of immunology research2026

Metabolic Reprogramming of T Cells by MSCs Rebalances Th17/Treg Axis to Attenuate Collagen-Induced Arthritis.

Xiaoping Wang, Jingjing He, Qun Wang, Xue Liu, Haoming Yuan, Lu Jin, Meng Ding, Lin Yang, Shaoxin Cui, Fei Chang and 6 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of immunology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

16 authors.

Xiaoping WangDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0003-4077-4465
Jingjing HeHebei International Joint Research Center on Rheumatic Diseases, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0000-0002-7936-3730
Qun WangDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0008-2203-9789
Xue LiuDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0007-3520-3237
Haoming YuanDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0000-0003-4099-0515
Lu JinDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0004-3282-233X
Meng DingDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0009-8452-1279
Lin YangDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0008-3356-1951
Shaoxin CuiDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0002-9515-0919
Fei ChangDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0000-0001-6249-3988
Tong XinDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0000-0003-2073-7731
Hongtao JinDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0008-4455-671X
Min ShiHebei International Joint Research Center on Rheumatic Diseases, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.
Yongzhou SongDepartment of Orthopedics, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0001-0092-396X
Wensen PanDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0009-0006-4398-4523
Aijing LiuDepartment of Rheumatology and Immunology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, China, hebmu.edu.cn.ORCID https://orcid.org/0000-0002-5762-5592

Funding

Government Foundation of Excellent Clinical Medicine Talent Program of Hebei ZF2025100Hebei Province Medical Science Research Key Project 20240127Natural Science Foundation of Hebei Province H2023206264
6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by dysregulated T cell responses and metabolic disturbances. Mesenchymal stromal cells (MSCs) have shown therapeutic promise, but their mechanisms, particularly concerning T cell metabolism, remain incompletely defined. This study investigated whether human umbilical cord-derived MSCs (hUC-MSCs) ameliorate collagen-induced arthritis (CIA) by modulating T cell metabolism and differentiation.

methodsCIA was induced in DBA/1 mice. Animals received PBS or hUC-MSCs on day 28. Arthritis index (AI), joint histology, serum cytokines (TNF-α, IL-6, IL-17, and TGF-β), and metabolites (lactate and pyruvate) were assessed. Splenic T cell transcription factors (FOXP3, RORγt, and PU.1) and glycolytic genes (GLUT1, G6PD, and PFKFB3) were analyzed by real-time quantitative polymerase chain reaction (RT-qPCR) and western blot. In vitro, human CD4

resultsMSC treatment significantly attenuated arthritis severity, joint destruction, and splenomegaly in CIA mice. It reduced serum pro-inflammatory cytokines and normalized elevated lactate and pyruvate levels. In the spleen, MSCs suppressed RORγt and PU.1 while enhancing FOXP3 expression, and downregulated GLUT1 and G6PD mRNA. Positive correlations were found between glycolytic markers (GLUT1 and G6PD) and pro-inflammatory transcription factors (RORγt and PU.1), and between serum lactate and inflammatory cytokines. In vitro, hUC-MSCs directly inhibited Th17 differentiation and promoted Treg generation in human CD4

conclusionshUC-MSCs ameliorate CIA by restoring the Th17/Treg balance through metabolic reprogramming of T cells, specifically by suppressing glycolysis. This immunometabolic mechanism highlights the therapeutic potential of MSCs in RA.

Indexed as

Arthritis, ExperimentalArthritis, RheumatoidMesenchymal Stem CellsMesenchymal Stem Cell TransplantationTh17 CellsT-Lymphocytes, RegulatoryAnimalsCell DifferentiationCells, CulturedCoculture TechniquesCytokinesDisease Models, AnimalGlycolysisHumansMaleMetabolic ReprogrammingCytokinescollagen-induced arthritisglycolysismesenchymal stromal cellsrheumatoid arthritisT cell metabolismTh17/Treg balance

Identifiers

PMID42260739
PMCPMC13247138

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Registered trials

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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.