Evidence map›Paper›PMID 33446887›Full record

ArticleCellular & molecular immunology2021

Induced regulatory T cells suppress Tc1 cells through TGF-β signaling to ameliorate STZ-induced type 1 diabetes mellitus.

Li Zhou, Xuemin He, Peihong Cai, Ting Li, Rongdong Peng, Junlong Dang, Yue Li, Haicheng Li, Feng Huang, Guojun Shi and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. TGF-β signaling mediates crosstalk between CD8Journal of biomedical science · 2026
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Unveiling cell subpopulations in T1D mouse islets using single-cell RNA sequencing.American journal of physiology. Endocrinology and metabolism · 2024
    Article
  9. Effect of pegagan (Narra J · 2024
    Article
  10. Modulation of CXCL10 activity as a therapeutic target of ocular toxoplasmosis in diabetic mice.Journal of parasitic diseases : official organ of the Indian Society for Parasitology · 2024
    Article
  11. Article
  12. Review
  13. 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

13 authors at 1 institution in 1 country.

Li ZhouDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Xuemin HeDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Peihong CaiDepartment of Clinical Immunology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Ting LiDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Rongdong PengDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Junlong DangDepartment of Clinical Immunology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Yue LiDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Haicheng LiDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Feng HuangDepartment of Clinical Immunology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Guojun ShiDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Chichu XieDepartment of Clinical Immunology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China.
Yan LuDepartment of Clinical Immunology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China. luyan36@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0002-5893-6114
Yanming ChenDepartment of Endocrinology and Metabolism, Guangdong Provincial Key Laboratory of Diabetology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, Guangdong, China. chyanm@mail.sysu.edu.cn.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes mellitus (T1D) is a chronic autoimmune condition in which the immune system destroys insulin-producing pancreatic β cells. In addition to well-established pathogenic effector T cells, regulatory T cells (Tregs) have also been shown to be defective in T1D. Thus, an increasing number of therapeutic approaches are being developed to target Tregs. However, the role and mechanisms of TGF-β-induced Tregs (iTregs) in T1D remain poorly understood. Here, using a streptozotocin (STZ)-induced preclinical T1D mouse model, we found that iTregs could ameliorate the development of T1D and preserve β cell function. The preventive effect was associated with the inhibition of type 1 cytotoxic T (Tc1) cell function and rebalancing the Treg/Tc1 cell ratio in recipients. Furthermore, we showed that the underlying mechanisms were due to the TGF-β-mediated combinatorial actions of mTOR and TCF1. In addition to the preventive role, the therapeutic effects of iTregs on the established STZ-T1D and nonobese diabetic (NOD) mouse models were tested, which revealed improved β cell function. Our findings therefore provide key new insights into the basic mechanisms involved in the therapeutic role of iTregs in T1D.

Indexed as

Gene Expression RegulationAnimalsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1FemaleHepatocyte Nuclear Factor 1-alphaInsulin-Secreting CellsMaleMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutT-Lymphocytes, CytotoxicT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesTransforming Growth Factor betaHepatocyte Nuclear Factor 1-alphaHnf1a protein, mousemTOR protein, mouseTOR Serine-Threonine KinasesTransforming Growth Factor betainduced regulatory T cellsmTOR and TCF1TGF-βtype 1 cytotoxic T cellstype 1 diabetes mellitus

Identifiers

PMID33446887
PMCPMC8027661
OpenAlexW3118692466

What OpenQuestion holds

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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.