Evidence map›Paper›PMID 39934569›Full record

ArticleImmunologic research2025

Metformin suppresses gammadelta T17 cell differentiation alleviating DSS-induced colitis.

Mingzhong Sun, Hongli Liu, Huixiang Ju, Hongmei Chen, Rui Yang, Dongmei Yan, Langping Shen, Aiting Cai, Yaru Zhi, Lihua Xiao and 2 more

Abstract read
In one paragraph

Article in Immunologic research, 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. 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.

Mingzhong Sun *Department of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Hongli Liu *Department of Laboratory Medicine, Nantong Tumor Hospital, Tumor Hospital Affiliated to Nantong University, Nantong, 226000, Jiangsu, China.
Huixiang Ju *Department of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Hongmei ChenDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Rui YangDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Dongmei YanDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Langping ShenDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Aiting CaiDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Yaru ZhiDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Lihua XiaoDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Qinfang TangDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China.
Yungang WangDepartment of Laboratory Medicine, Affiliated Hospital 6 of Nantong University, Yancheng Third People' S Hospital, The Yancheng School of Clinical Medicine of Jiangsu Vocational College of Medicine, The Yancheng School of Clinical Medicine of Nanjing Medical University, Yancheng, 224000, Jiangsu, China. wyg1223@126.com.

Funding

Clinical Medicine Special Research Foundation of Nantong University 2023JZ020Collaborative Innovation Research Project of Jiangsu Vocational College of Medicine 202490101Natural Science Foundation of China 81902906The Natural Science Foundation of Jiangsu Province SBK20241852The Natural Science Foundation of Yancheng City YCBK2024019
6 · The paper itself

Abstract

Ulcerative colitis (UC) is a chronic, nonspecific, relapsing inflammatory bowel disease. Metformin has pleiotropic effects including anti-inflammatory properties and a notable impact on the gut microbiome. γδT17 cells play crucial role in initiating and maintaining intestinal inflammation. The effect of metformin on γδT17 cells remains unclear. This study aims to explore the connection between metformin-mediated ameliorated response in colitis mice and γδT17 cell activity. The role of γδT17 cell inhibition in metformin-mediated colitis amelioration was evaluated in mice. The effect of metformin on γδT17 differentiation and the possible mechanism were evaluated in a set of in vitro experiments. Results showed that the accumulation of γδT17 cells was negatively correlated with metformin treatment in DSS-induced colitis mice. Exogenous γδT17 cells blocked metformin-mediated colitis inhibition. Furthermore, metformin inhibited γδT17 differentiation, which was related to the inhibition of mTOR/RORγt activity. Our results reveal that metformin ameliorates colitis symptoms by suppressing γδT17 differentiation, suggesting a viable strategy against UC, although the mechanism of metformin in inhibiting γδT17 differentiation remains to be further studied.

Indexed as

ColitisColitis, UlcerativeMetforminReceptors, Antigen, T-Cell, gamma-deltaTh17 CellsAnimalsCell DifferentiationCells, CulturedDextran SulfateDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLNuclear Receptor Subfamily 1, Group F, Member 3TOR Serine-Threonine KinasesDextran SulfateMetforminNuclear Receptor Subfamily 1, Group F, Member 3Receptors, Antigen, T-Cell, gamma-deltaTOR Serine-Threonine KinasesMetforminUlcerative colitisγδT17 cell

Identifiers

PMID39934569
PMCPMC11813991

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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.