Evidence map›Paper›PMID 27619885›Full record

ArticleJournal of experimental & clinical cancer research : CR2016

Tumoricidal efficacy coincides with CD11c up-regulation in antigen-specific CD8(+) T cells during vaccine immunotherapy.

Yohei Takeda, Masahiro Azuma, Misako Matsumoto, Tsukasa Seya

Open access · goldAbstract read
In one paragraph

Article in Journal of experimental & clinical cancer research : CR, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 24 citations in OpenAlex.

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  9. Review
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  11. Decreased granzyme-B expression in CD11cFrontiers in immunology · 2023
    Article
  12. Article
  13. Host-pathogen protein-nucleic acid interactions: A comprehensive review.Computational and structural biotechnology journal · 2022
    Review
  14. HIV-1-Specific CD11cFrontiers in immunology · 2021
    Article
  15. Article
  16. Article
  17. Article
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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 1 institution in 1 country.

Yohei TakedaDepartment of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita 15, Nishi 7, Kita-ku, Sapporo, 060-8638, Japan.
Masahiro AzumaDepartment of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita 15, Nishi 7, Kita-ku, Sapporo, 060-8638, Japan.
Misako MatsumotoDepartment of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita 15, Nishi 7, Kita-ku, Sapporo, 060-8638, Japan.
Tsukasa SeyaDepartment of Microbiology and Immunology, Hokkaido University Graduate School of Medicine, Kita 15, Nishi 7, Kita-ku, Sapporo, 060-8638, Japan. seya-tu@pop.med.hokudai.ac.jp.
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDendritic cells (DCs) mount tumor-associated antigens (TAAs), and the double-stranded RNA adjuvant Poly(I:C) stimulates Toll-like receptor 3 (TLR3) signal in DC, which in turn induces type I interferon (IFN) and interleukin-12 (IL-12), then cross-primes cytotoxic T lymphocytes (CTLs). Proliferation of CTLs correlates with tumor regression. How these potent cells expand with high quality is crucial to the outcome of CTL therapy. However, good markers reflecting the efficacy of DC-target immunotherapy have not been addressed.

methodsUsing an EG7 (ovalbumin, OVA-positive) tumor-implant mouse model, we examined what is a good marker for active CTL induction in treatment with Poly(I:C)/OVA.

resultsSimultaneous administration of Poly(I:C) and antigen (Ag) OVA significantly increased a minor population of CD8(+) T cells, that express CD11c in lymphoid and tumor sites. The numbers of the CD11c(+) CD8(+) T cells correlated with those of induced Ag-specific CD8(+) T cells and tumor regression. The CD11c(+) CD8(+) T cell moiety was characterized by its high killing activity and IFN-γ-producing ability, which represent an active phenotype of the effector CTLs. Not only a TLR3-specific (TICAM-1-dependent) signal but also TLR2 (MyD88) signal in DC triggered the expansion of CD11c(+) CD8(+) T cells in tumor-bearing mice. Notably, human CD11c(+) CD8(+) T cells also proliferated in peripheral blood mononuclear cells (PBMC) stimulated with cytomegalovirus (CMV) Ag.

conclusionsCD11c expression in CD8(+) T cells reflects anti-tumor CTL activity and would be a marker for immunotherapeutic efficacy in mouse models and probably cancer patients as well.

Indexed as

AnimalsCancer VaccinesCD11c AntigenCD8-Positive T-LymphocytesDendritic CellsGene Expression Regulation, NeoplasticHumansImmunotherapyMiceMice, Inbred C57BLNeoplasms, ExperimentalOvalbuminPoly I-CUp-RegulationXenograft Model Antitumor AssaysCancer VaccinesCD11c AntigenOvalbuminPoly I-CAdjuvantAntitumor immunotherapyCD11c+ CD8+ T cellCTLPoly(I:C)Therapeutic markerTLR3

Identifiers

PMID27619885
PMCPMC5020536
OpenAlexW2520382278

What OpenQuestion holds

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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.