Evidence map›Paper›PMID 25430879›Full record

ArticleCancer gene therapy2014

Type I IFN gene delivery suppresses regulatory T cells within tumors.

H Hashimoto, R Ueda, K Narumi, Y Heike, T Yoshida, K Aoki

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Cancer gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

33 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Targeting cytokine and chemokine signaling pathways for cancer therapy.Signal transduction and targeted therapy · 2024
    Review
  5. Article
  6. Review
  7. Recent Advances of RNA mCancer treatment and research · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Type I interferon-mediated tumor immunity and its role in immunotherapy.Cellular and molecular life sciences : CMLS · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Local memory CD4 T cell niches in respiratory viral infection.The Journal of experimental medicine · 2021
    Article
  18. Review
  19. Review
  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 1 institution in 1 country.

H HashimotoDivision of Gene and Immune Medicine, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
R UedaDivision of Gene and Immune Medicine, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
K NarumiDivision of Gene and Immune Medicine, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Y HeikeDivision of Cancer Immunotherapy, Exploratory Oncology Research & Clinical Trial Center, Chuo-ku, Tokyo, Japan.
T YoshidaDivision of Genetics, National Cancer Center Research Institute, National Cancer Center, Chuo-ku, Tokyo, Japan.
K AokiDivision of Gene and Immune Medicine, National Cancer Center Research Institute, Chuo-ku, Tokyo, Japan.
Japan Clinical Cancer Research Organization · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferon (IFN) is a pleiotropic cytokine regulating the cancer cell death and immune response. IFN-α can, as we have also reported, effectively induce an antitumor immunity by the activation of tumor-specific T cells and maturation of dendritic cells in various animal models. Unknown, however, is how the type I IFN alters the immunotolerant microenvironment in the tumors. Here, we found that intratumoral IFN-α gene transfer significantly decreased the frequency of regulatory T cells (Tregs) per CD4(+) T cells in tumors. The concentration of a Treg-inhibitory cytokine, interleukin (IL)-6, was correlated with the IFN-α expression level in tumors, and intratumoral CD11c(+) cells produced IL-6 in response to IFN-α stimulation. To confirm the role of IL-6 in the suppression of Tregs in tumors, an anti-IL-6 receptor antibody was administered in IFN-α-treated mice. The antibody increased the frequency of Tregs in the tumors, and attenuated systemic tumor-specific immunity induced by IFN-α. Furthermore, the IFN-α-mediated IL-6 production increased the frequency of Th17 cells in the tumors, which may be one of the mechanisms for the reduction of Tregs. The study demonstrated that IFN-α gene delivery creates an environment strongly supporting the enhancement of antitumor immunity through the suppression of Tregs.

Indexed as

AdenoviridaeAnimalsCell Line, TumorDisease ProgressionGene ExpressionGenetic TherapyGenetic VectorsGene Transfer TechniquesHumansImmunomodulationInterferon-alphaInterferon Type IInterleukin-6Lymphocyte CountLymphocytes, Tumor-InfiltratingMaleInterferon-alphaInterferon Type IInterleukin-6Receptors, Interleukin-6

Identifiers

PMID25430879
OpenAlexW2083850389

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.