Evidence map›Paper›PMID 11529935›Full record

ArticleImmunology2001

Interleukin-10 expressed at early tumour sites induces subsequent generation of CD4(+) T-regulatory cells and systemic collapse of antitumour immunity.

N Seo, S Hayakawa, M Takigawa, Y Tokura

Open access · greenAbstract read
In one paragraph

Article in Immunology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.

  1. Relationship Between Interleukin-10 Gene C-819T Polymorphism and Gastric Cancer Risk: Insights From a Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Pooled it
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  4. Induction of robust type-I CD8+ T-cell responses in WHO grade 2 low-grade glioma patients receiving peptide-based vaccines in combination with poly-ICLC.Clinical cancer research : an official journal of the American Association for Cancer Research · 2015
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  6. Article
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  11. Targeting glycans for CAR therapy: The advent of sweet CARs.Molecular therapy : the journal of the American Society of Gene Therapy · 2022
    Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Clinical Application of Cytokines in Cancer Immunotherapy.Drug design, development and therapy · 2021
    Review
  17. Review
  18. Review
  19. Review
  20. Article

1 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

4 authors at 2 institutions in 1 country.

N SeoDepartment of Dermatology, Hamamatsu University School of Medicine, Shizuoka, Japan. seo445@hama-med.ac.jp
S Hayakawa
M Takigawa
Y Tokura
Hamamatsu University School of Medicine · JPNihon University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the relationship between transforming growth factor-beta (TGF-beta)-secreting T-regulatory (Tr) cells and anti-B16 melanoma immunity, and studied the association of early cytokines expressed at tumour sites with the generation of Tr cells. A large number of CD4(+) Tr cells producing interleukin (IL)-4, IL-10 and TGF-beta accumulated with functionally depressed CD8(+) cytotoxic T lymphocytes (CTLs) at tumour sites on day 20 after subcutaneous (s.c.) inoculation of B16 tumour cells. Tr cells consisted of two populations, which were termed T helper 3 (Th3) and Tr1 cells. B16-infiltrating Tr cells strongly inhibited the generation of B16-specific T helper 1 (Th1) cells in a TGF-beta-dependent manner and were assumed to suppress effective generation of CTLs. In addition, B16 cells markedly progressed in mice transferred adoptively by the cultured B16-infiltrating Tr cells compared with untreated mice. The capacity of these Tr cells to produce TGF-beta was hampered by neutralizing anti-IL-10 and partly anti-IL-4 monoclonal antibodies (mAbs) injected intralesionally during the early development of B16 tumours, and this treatment markedly attenuated B16 growth. Furthermore, a lesional injection of recombinant mouse IL-10 at an early tumour site resulted in the vigorous progression of B16 tumours. These results provide evidence that Tr cells, belonging to the T helper 3/T-regulatory 1 (Th3/Tr1) type, are activated in B16-bearing hosts under the influence of T helper 2 (Th2) cytokines, mainly IL-10 (produced at early tumour lesions), and that this regulatory T-cell population functions as a suppressor of anti-B16 immunity.

Indexed as

Immune ToleranceAnimalsCD4-Positive T-LymphocytesCell Culture TechniquesDisease ProgressionDown-RegulationFemaleImmunity, CellularInterleukin-10Lymphocytes, Tumor-InfiltratingMelanoma, ExperimentalMiceMice, Inbred C57BLT-Lymphocyte SubsetsTransforming Growth Factor betaInterleukin-10Transforming Growth Factor beta

Identifiers

PMID11529935
PMCPMC1783257
OpenAlexW2059762191

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.