Evidence map›Paper›PMID 25070361›Full record

ArticleClinical and experimental immunology2014

Mesenchymal stem cells suppress CD8+ T cell-mediated activation by suppressing natural killer group 2, member D protein receptor expression and secretion of prostaglandin E2, indoleamine 2, 3-dioxygenase and transforming growth factor-β.

Mingfen Li, Xuyong Sun, Xiaocong Kuang, Yan Liao, Haibin Li, Dianzhong Luo

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

49 citing papers in PubMed, 73 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Stem cell therapy in systemic sclerosis.Clinical rheumatology · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. 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

6 authors at 4 institutions in 1 country.

Mingfen LiDepartment of Pathology, First Affiliated Hospital of Guangxi Medical University, Nanning, China; Clinical Laboratory, First Affiliated Hospital of the University of Chinese Medicine in Guangxi, Nanning, China.
Xuyong Sun
Xiaocong Kuang
Yan Liao
Haibin Li
Dianzhong Luo
Guangxi Medical University · CN303 Hospital of People's Liberation Army · CNFirst Affiliated Hospital of GuangXi Medical University · CNGeneral Hospital of Guangzhou Military Command · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bone marrow mesenchymal stem cells (BMSCs) inhibit immune cell responsiveness, and especially of T lymphocytes. We showed that BMSCs markedly inhibited the proliferation and cytokine production by CD8(+) T cells by a cell-to-cell contact phenomenon and secretion of soluble factors. BMSCs down-regulate the expression of natural killer group 2, member D protein (NKG2D) receptors on CD8(+) T cells when co-cultured with them. Moreover, CD8(+) T cells that express low levels of NKG2D had impaired proliferation after triggering by a mitogen. The major histocompatibility complex (MHC) class I chain-related (MIC) A/B molecule, which is a typical ligand for NKG2D, was expressed on BMSCs, and caused dampening of cell proliferation. Monoclonal antibody blocking experiments targeted to MIC A/B impaired CD8(+) T cell function, as evaluated by proliferation and cytokine production. In addition, the production of prostaglandin E2 (PGE2 ), indoleamine 2, 3-dioxygenase (IDO) and transforming growth factor (TGF)-β1 were increased when BMSCs were co-cultured with CD8(+) T cells. The addition of specific inhibitors against PGE2 , IDO and TGF-β partially restored the proliferation of CD8(+) T cells. Our results suggest that BMSCs suppress CD8(+) T cell-mediated activation by suppressing NKG2D expression and secretion of PGE2, IDO and TGF-β. Our observations further confirm the feasibility of BMSCs as a potential adoptive cellular therapy in immune-mediated diseases such as graft-versus-host disease (GVHD).

Indexed as

Lymphocyte ActivationCD8-Positive T-LymphocytesCell CommunicationCells, CulturedDinoprostoneGranzymesHistocompatibility Antigens Class IHumansIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaInterleukin-2Mesenchymal Stem CellsNK Cell Lectin-Like Receptor Subfamily KTransforming Growth Factor betaDinoprostoneGranzymesHistocompatibility Antigens Class IIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaInterleukin-2KLRK1 protein, humanMHC class I-related chain ANK Cell Lectin-Like Receptor Subfamily KTransforming Growth Factor betaCD8+ T lymphocytesimmunosuppressionmesenchymal stem cellNKG2Dsoluble factor

Identifiers

PMID25070361
PMCPMC4238878
OpenAlexW1779998146

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.