Evidence map›Paper›PMID 38773213›Full record

ArticleScientific reports2024

Treg-derived TGF-β1 dampens cGAS-STING signaling to downregulate the expression of class I MHC complex in multiple myeloma.

Disi Zhang, Dong Zhan, Rui Zhang, Yunyan Sun, Ci Duan, Jiapeng Yang, Jia Wei, Xianshi Li, Yanqi Lu, Xun Lai

Abstract read
In one paragraph

Article in Scientific reports, 2024. 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
–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

17 citing papers in PubMed.

  1. Review
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  4. ROS-Responsive MnOJournal of nanobiotechnology · 2026
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  7. Review
  8. Review
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  13. STING Agonists and How to Reach Their Full Potential in Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  14. Article
  15. Review
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  17. 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

10 authors.

Disi Zhang *Department of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Dong Zhan *Department of Human Anatomy and Histology and Embrology, School of Basic Medical Sciences, Kunming Medical University, Kunming, Yunnan Province, China.
Rui ZhangDepartment of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Yunyan SunDepartment of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Ci DuanDepartment of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Jiapeng YangDepartment of Thoracic Surgery, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Jia WeiDepartment of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Xianshi LiDepartment of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Yanqi LuDepartment of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China.
Xun LaiDepartment of Hematology, Yunnan Cancer Hospital, The Third Affiliated Hospital of Kunming Medical University, Peking University Cancer Hospital Yunnan, No. 519 Kunzhou Road, Xishan District, Kunming, Yunnan Province, China. laixun2021@163.com.

Funding

Kunming Joint Special Project 202001AC070202Kunming Joint Special Project 202001AC070617National Natural Science Foundation of China 8216010239Qiu Lu Gui Expert Workstation in Yunnan Province 202105AF150051The Joint Project of Kunming Medical University and Science and Technology Agency 202101AY070001-049Yunnan Fundamental Research Projects 202101AT070199
6 · The paper itself

Abstract

Multiple myeloma (MM) progression involves diminished tumor antigen presentation and an immunosuppressive microenvironment, characterized by diminished expression of major histocompatibility complexes (MHC) class I molecule and elevated programmed death ligand 1 (PDL1) in MM cells, along with an enriched population of regulatory T cells (Tregs). To investigate Treg's influence on MM cells, we established a co-culture system using Tregs from MM patients and the MM cell lines (MM.1S and SK-MM-1) in vitro and assessed the effects of intervening in the relevant pathways connecting Tregs and MM cells in vivo. In vitro, Tregs induced transforming growth factor beta-1 (TGF-β1) production, downregulated MHC I members, and increased PDL1 expression in MM cells. Treg-derived TGF-β1 suppressed the cGAS-STING pathway, contributing to the loss of MHC I molecule expression and PDL1 upregulation. Correspondingly, neutralizing TGF-β1 or activating the cGAS-STING pathway restored MHC I and PDL1 expression, effectively countering the pro-tumorigenic effect of Tregs on MM cells in vivo. These data elucidated how Tregs influence tumor antigen presentation and immunosuppressive signal in MM cells, potentially providing therapeutic strategies, such as neutralizing TGF-β1 or activating the cGAS-STING pathway, to address the immune escape and immunosuppressive dynamics in MM.

Indexed as

B7-H1 AntigenHistocompatibility Antigens Class IMembrane ProteinsMultiple MyelomaNucleotidyltransferasesSignal TransductionT-Lymphocytes, RegulatoryTransforming Growth Factor beta1AnimalsCell Line, TumorCoculture TechniquesCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDown-RegulationFemaleGene Expression Regulation, NeoplasticHumansB7-H1 AntigenCD274 protein, humancGAS protein, humanCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseHistocompatibility Antigens Class IMembrane ProteinsNucleotidyltransferasesTGFB1 protein, humanTransforming Growth Factor beta1cGAS-STINGMajor histocompatibility complexes (MHC)Multiple myeloma (MM)Regulatory T cell (Treg)TGF-β1

Identifiers

PMID38773213
PMCPMC11109281

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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.