Evidence map›Paper›PMID 24777831›Full record

ArticleEuropean journal of immunology2014

PIAS1 and STAT-3 impair the tumoricidal potential of IFN-γ-stimulated mouse dendritic cells generated with IL-15.

Neale T Hanke, Collin J LaCasse, Claire B Larmonier, Darya Alizadeh, Malika Trad, Nona Janikashvili, Bernard Bonnotte, Emmanuel Katsanis, Nicolas Larmonier

Open access · greenAbstract read
In one paragraph

Article in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
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

9 authors at 4 institutions in 2 countries.

Neale T Hanke *Department of Pediatrics, University of Arizona, Tucson, AZ, United States of America.
Collin J LaCasse *Department of Pediatrics, University of Arizona, Tucson, AZ, United States of America.
Claire B LarmonierDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States of America.
Darya AlizadehDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States of America.
Malika TradINSERM UMR 1098, Faculty of Medicine, Dijon, France.
Nona JanikashviliINSERM UMR 1098, Faculty of Medicine, Dijon, France.
Bernard BonnotteINSERM UMR 1098, Faculty of Medicine, Dijon, France.
Emmanuel KatsanisDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States of America.
Nicolas LarmonierDepartment of Pediatrics, University of Arizona, Tucson, AZ, United States of America.
University of Arizona · USUniversité de Bourgogne · FRInserm · FRZero to Three · US

Funding

VITAMIN AP30CA023074 · NCI · UNIVERSITY OF ARIZONA · PI Dan Theodorescu · 1985 to 2026
$110.2M
Integrative Cancer Scholars Training GrantT32CA009213 · NCI · UNIVERSITY OF ARIZONA · PI CAREW, JENNIFER S, CURIEL-LEWANDROWSKI, CLARA · 1985 to 2024
$8.6M
Immunotherapy for Chronic Myelogenous LeukemiaR01CA104926 · NCI · UNIVERSITY OF ARIZONA · PI KATSANIS, EMMANUEL · 2004 to 2013
$2.4M
NCI NIH HHS CA023074NCI NIH HHS P30 CA023074NCI NIH HHS R01 CA104926NCI NIH HHS T32 CA009213NCI NIH HHS T32CA009213
6 · The paper itself

Abstract

Primarily defined by their antigen-presenting property, dendritic cells (DCs) are being implemented as cancer vaccines in immunotherapeutic interventions. DCs can also function as direct tumor cell killers. How DC cytotoxic activity can be efficiently harnessed and the mechanisms controlling this nonconventional property are not fully understood. We report here that the tumoricidal potential of mouse DCs generated from myeloid precursors with GM-CSF and IL-15 (IL-15 DCs) can be triggered with the Toll-like receptor (TLR) 4 ligand lipopolysaccharide to a similar extent compared with that of their counterparts, conventionally generated with IL-4 (IL-4 DCs). The mechanism of tumor cell killing depends on the induction of iNOS expression by DCs. In contrast, interferon (IFN)-γ induces the cytotoxic activity of IL-4 but not IL-15 DCs. Although the IFN-γ-STAT-1 signaling pathway is overall functional in IL-15 DCs, IFN-γ fails to induce iNOS expression in these cells. iNOS expression is negatively controlled in IFN-γ-stimulated IL-15 DCs by the cooperation between the E3 SUMO ligase PIAS1 and STAT-3, and can be partially restored with PIAS1 siRNA and STAT-3 inhibitors.

Indexed as

AnimalsCell Line, TumorDendritic CellsFemaleGranulocyte-Macrophage Colony-Stimulating FactorInterferon-gammaInterleukin-15Interleukin-4LigandsLipopolysaccharidesMiceMice, Inbred BALB CMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIProtein Inhibitors of Activated STATGranulocyte-Macrophage Colony-Stimulating FactorInterferon-gammaInterleukin-15Interleukin-4LigandsLipopolysaccharidesNitric OxideNitric Oxide Synthase Type IINos2 protein, mousePias1 protein, mouseProtein Inhibitors of Activated STATStat1 protein, mouseSTAT1 Transcription FactorStat3 protein, mouseSTAT3 Transcription FactorTlr4 protein, mouseToll-Like Receptor 4Cytotoxic dendritic cellsiNOSNF-κBPIAS1STAT-3

Identifiers

PMID24777831
PMCPMC4141036
OpenAlexW1893697448

What OpenQuestion holds

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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.