Evidence map›Paper›PMID 30629318›Full record

ArticleCancer science2019

Soluble factors derived from neuroblastoma cell lines suppress dendritic cell differentiation and activation.

Kazuaki Harada, Fumie Ihara, Mariko Takami, Toshiko Kamata, Naoko Mise, Hiroko Yoshizawa, Tomoro Hishiki, Takeshi Saito, Keita Terui, Mitsuyuki Nakata and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 16 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

15 authors at 3 institutions in 1 country.

Kazuaki HaradaDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Fumie IharaDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Mariko TakamiDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Toshiko KamataDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Naoko MiseDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Hiroko YoshizawaDepartment of Medical Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan.
Tomoro HishikiDivision of Surgical Oncology, Children's Cancer Center, National Center for Child Health and Development, Tokyo, 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.
Mitsuyuki NakataDepartment of Pediatric Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan.
Shugo KomatsuDepartment 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.ORCID https://orcid.org/0000-0002-9332-3129
Chiba University · JPChiba University Hospital · JPNational Center For Child Health and Development · JP

Funding

Japan Society for the Promotion of Science #18K16274Japan Society for the Promotion of Science #25861664
6 · The paper itself

Abstract

Dendritic cells (DC) play a key role in the initiation of both antitumor immunity and immunological tolerance. It has been demonstrated that exposure to soluble factors produced by tumor cells modulates DC functions and induces tolerogenic DC differentiation. In this study, we investigated the effects of neuroblastoma cell line-derived soluble factors on DC differentiation. Monocytes isolated from healthy volunteers were incubated with interleukin (IL)-4 and granulocyte-macrophage colony-stimulating factor in the presence of culture supernatants from neuroblastoma cell lines. The culture supernatants from neuroblastoma cell lines, such as NLF and GOTO, partially blocked both downregulation of CD14 and upregulation of CD1a, and dramatically decreased IL-12 and tumor necrosis factor (TNF)-α production from mature DC, while no effect of SH-SY5Y cell supernatant was noted. In addition, IL-6 and IL-10 production from monocytes was increased by the supernatants of NLF and GOTO cells at 24 hours after incubation. Furthermore, we evaluated DC functions through stimulation of invariant natural killer T (iNKT) cells. α-Galactosylceramide-pulsed DC co-cultured with supernatants of NLF cells were unable to sufficiently stimulate iNKT cells. The decreased ability of iNKT cells to produce interferon (IFN)-γ after stimulation with neuroblastoma cell line supernatant-cultured DC was reversed by addition of IL-12. CD40 expression and IL-12 production in NLF-sup-treated DC were increased by addition of exogenous IFN-γ. These results indicate that tolerogenic DC are induced in the neuroblastoma tumor microenvironment and attenuate the antitumor effects of iNKT cells. Interactions between iNKT cells and αGalCer-pulsed DC have the potential to restore the immunosuppression of tolerogenic DC through IFN-γ production.

Indexed as

Antigens, CD1Cell DifferentiationCell LineCell Line, TumorDendritic CellsGranulocyte-Macrophage Colony-Stimulating FactorHumansInterferon-gammaInterleukin-10Interleukin-12Interleukin-4Lipopolysaccharide ReceptorsLymphocyte ActivationMonocytesNeuroblastomaAntigens, CD1CD1a antigenGranulocyte-Macrophage Colony-Stimulating FactorInterferon-gammaInterleukin-10Interleukin-12Interleukin-4Lipopolysaccharide Receptorsdendritic cellsimmunosuppressioninvariant natural killer T cellneuroblastoma

Identifiers

PMID30629318
PMCPMC6398884
OpenAlexW2909738847

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.