Evidence map›Paper›PMID 28099147›Full record

ArticleOncotarget2017

CTLA-4 positive breast cancer cells suppress dendritic cells maturation and function.

Xi Chen, Qianqian Shao, Shengnan Hao, Zhonghua Zhao, Yang Wang, Xiaofan Guo, Ying He, Wenjuan Gao, Haiting Mao

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
3.8field-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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. CTLA-4 Expression and Its Clinical Significance in Breast Cancer.Archivum immunologiae et therapiae experimentalis · 2021
    Pooled it
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. CD8Frontiers in immunology · 2024
    Review
  20. Article

2 more citing papers are in PubMed but not listed here.

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

9 authors at 1 institution in 1 country.

Xi ChenInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Qianqian ShaoInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Shengnan HaoInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Zhonghua ZhaoInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Yang WangInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Xiaofan GuoDepartment of Neurosurgery, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Ying HeInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Wenjuan GaoInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Haiting MaoInstitute of Basic Medicial Sciences, Qi Lu Hospital, Shandong University, Jinan, Shandong Province, 250012, P.R.China.
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cytotoxic T lymphocyte-associated antigen 4 (CTLA-4), a potent immunoregulatory molecule, can down-regulate T-cell activation and inhibit anti-tumor immune response. This study showed that LPS-stimulated human dendritic cells (DCs) decreased the expression of HLA-DR, CD83 and costimulatory molecules (CD40, CD80 and CD86) following coculturing with CTLA-4+ breast cancer cells. Moreover, the suppressed DCs further inhibited proliferation of allogeneic CD4+/CD8+ T-cells, differentiation of Th1 and function of cytotoxic lymphocytes (CTLs). However, CTLA-4 blockade in breast cancer cells could recover DC maturation and cytokine production, elevate antigen-presenting function of DCs, reverse Th1/CTLs response and cytokine secretion. Subsequent study demonstrated that the activation of extracellular-signal regulated kinase and signal transducer and activator of transcription 3 of DCs caused by CTLA-4+ breast cancer cells were the predominant mechanism of DC suppression. In addition, CTLA-4 blockade treatment also directly inhibited proliferation and induced apoptosis of CTLA-4+ breast cancer cells. Collectively, CTLA-4 was expressed and functional on human breast cancer cells through influencing maturation and function of DCs in vitro, and CTLA-4 blockage not only recovered the antigen-presenting function of DCs and T-cells activation but also suppressed the biological activity of breast cancer cells themselves. This study highlights the clinical application of CTLA-4 blockade therapy in breast cancer.

Indexed as

Antigen PresentationBreast NeoplasmsCD4-Positive T-LymphocytesCTLA-4 AntigenCytokinesDendritic CellsFemaleFlow CytometryHumansMCF-7 CellsMonocytesTh1 CellsCTLA-4 AntigenCTLA4 protein, humanCytokinesbreast cancer cellCD4+T cellCD8+T cellCTLA-4dendritic cell

Identifiers

PMID28099147
PMCPMC5355131
OpenAlexW2571686442

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.