Evidence map›Paper›PMID 26749374›Full record

ArticleCancer science2016

Antibody-dependent cellular cytotoxicity toward neuroblastoma enhanced by activated invariant natural killer T cells.

Naoko Mise, Mariko Takami, Akane Suzuki, Toshiko Kamata, Kazuaki Harada, Tomoro Hishiki, Takeshi Saito, Keita Terui, Tetsuya Mitsunaga, Mitsuyuki Nakata and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

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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

14 authors at 3 institutions in 1 country.

Naoko MiseDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Mariko TakamiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Akane SuzukiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Toshiko KamataDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Kazuaki HaradaDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tomoro HishikiDepartment of Pediatric Surgery, Chiba Children's Hospital, Chiba, Japan.
Takeshi SaitoDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Keita TeruiDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tetsuya MitsunagaDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Mitsuyuki NakataDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Takayuki IkeuchiCenter for Advanced Medicine, Chiba University Hospital, Chiba, Japan.
Toshinori NakayamaDepartment of Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hideo YoshidaDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Shinichiro MotohashiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Chiba University · JPChiba Hospital · JPChiba University Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-ganglioside GD2 antibodies mainly work through antibody-dependent cellular cytotoxicity (ADCC) and have demonstrated clinical benefit for children with neuroblastoma. However, high-risk neuroblastoma still has a high recurrence rate. For further improvement in patient outcomes, ways to maximize the cytotoxic effects of anti-GD2 therapies with minimal toxicity are required. Activated invariant natural killer T (iNKT) cells enhance both innate and type I acquired anti-tumor immunity by producing several kinds of cytokines. In this report, we investigated the feasibility of combination therapy using iNKT cells and an anti-GD2 antibody. Although some of the expanded iNKT cells expressed natural killer (NK) cell markers, including FcγR, iNKT cells were not directly associated with ADCC. When co-cultured with activated iNKT cells, granzyme A, granzyme B and interferon gamma (IFNγ) production from NK cells were upregulated, and the cytotoxicity of NK cells treated with anti-GD2 antibodies was increased. Not only cytokines produced by activated iNKT cells, but also NK-NKT cell contact or NK cell-dendritic cell contact contributed to the increase in NK cell cytotoxicity and further IFNγ production by iNKT cells and NK cells. In conclusion, iNKT cell-based immunotherapy could be an appropriate candidate for anti-GD2 antibody therapy for neuroblastoma.

Indexed as

Antibody-Dependent Cell CytotoxicityAnimalsAntigens, CD1dCell Line, TumorCytokinesHumansLymphocyte ActivationMiceNatural Killer T-CellsNeuroblastomaAntigens, CD1dCD1D protein, humanCytokinesAntibody-dependent cellular cytotoxicityimmunotherapynatural killer cellsnatural killer T cellsneuroblastoma

Identifiers

PMID26749374
PMCPMC4814252
OpenAlexW2225671534

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.