Evidence map›Paper›PMID 27186393›Full record

ArticleAmerican journal of cancer research2016

Anti-CD40 antibody and toll-like receptor 3 ligand restore dendritic cell-mediated anti-tumor immunity suppressed by morphine.

Ming-Cheng Chang, Yu-Li Chen, Ying-Cheng Chiang, Ya-Jung Cheng, Yu-Wei Jen, Chi-An Chen, Wen-Fang Cheng, Wei-Zen Sun

Open access · greenAbstract read
In one paragraph

Article in American journal of cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
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  4. Opioid-Mediated HIV-1 Immunopathogenesis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  5. 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

8 authors at 2 institutions in 1 country.

Ming-Cheng ChangDepartment of Obstetrics and Gynecology, College of Medicine, National Taiwan UniversityTaipei, Taiwan; Department of Anesthesiology, College of Medicine, National Taiwan UniversityTaipei, Taiwan.
Yu-Li ChenDepartment of Obstetrics and Gynecology, National Taiwan University Hospital HsinChu Branch, HsihChu, Taiwan.
Ying-Cheng ChiangDepartment of Obstetrics and Gynecology, College of Medicine, National Taiwan University Taipei, Taiwan.
Ya-Jung ChengDepartment of Anesthesiology, College of Medicine, National Taiwan University Taipei, Taiwan.
Yu-Wei JenDepartment of Obstetrics and Gynecology, Cathay General Hospital Taipei, Taiwan.
Chi-An ChenDepartment of Obstetrics and Gynecology, College of Medicine, National Taiwan University Taipei, Taiwan.
Wen-Fang ChengDepartment of Obstetrics and Gynecology, College of Medicine, National Taiwan UniversityTaipei, Taiwan; Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan UniversityTaipei, Taiwan; Graduate Institute of Oncology, College of Medicine, National Taiwan UniversityTaipei, Taiwan.
Wei-Zen SunDepartment of Anesthesiology, College of Medicine, National Taiwan UniversityTaipei, Taiwan; Graduate Institute of Clinical Medicine, College of Medicine, National Taiwan UniversityTaipei, Taiwan.
National Taiwan University · TWCathay General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The influence of morphine on host immunity and the underlying mechanism are still unclear. In the current study, we investigated the influence of morphine on dendritic cells (DCs), its possible mechanism of action, and the molecules that could reverse these effects. Morphine suppressed DC maturation, antigen presenting abilities, and the ability to activate antigen-specific CD8(+) T cells. Morphine-treated DCs also secreted higher concentrations of IL-10, but lower IL-6 and TNF-α. Morphine-treated DCs showed decreased ERK1/2 phosphorylation and reduced p38 dephosphorylation. The in vivo administration of immuno-modulators, anti-CD40 Ab and TLR3 ligand-poly(I:C), enhanced antigen-specific immunity, promoted the anti-tumor effects, and prolonged the survival of morphine-treated, tumor-bearing mice by promoting the maturation and function of BMM-derived DCs by enhancing ERK1/2 phosphorylation and p38 dephosphorylation. We concluded that morphine can inhibit DC-mediated anti-tumor immunity by suppressing DC maturation and function. Immuno-modulators, such as anti-CD40 Abs and TLR agonists, can restore the DC-mediated anti-tumor immunity. Use of immuno-modulators could serve as a useful approach to overcome the immunocompromised state generated by morphine.

Indexed as

antigen presenting cellsantigen processinganti-tumor effectsdendritic cellsERK1/2 transduction pathwayimmune-modulatorimmunosuppressionMorphinep38 transduction pathway

Identifiers

PMID27186393
PMCPMC4859650
OpenAlexW2396807924

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.