Evidence map›Paper›PMID 26010746›Full record

ArticleImmunology and cell biology2016

Melanoma-derived factors alter the maturation and activation of differentiated tissue-resident dendritic cells.

Kristian M Hargadon, Johnathan D Bishop, John P Brandt, Zachary C Hand, Yonathan T Ararso, Osric A Forrest

Abstract read
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In one paragraph

Article in Immunology and cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

26 citing papers in PubMed, 45 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

6 authors at 1 institution in 1 country.

Kristian M HargadonHargadon Laboratory, Department of Biology, Hampden-Sydney College, Hampden-Sydney, VA, USA.
Johnathan D BishopHargadon Laboratory, Department of Biology, Hampden-Sydney College, Hampden-Sydney, VA, USA.
John P BrandtHargadon Laboratory, Department of Biology, Hampden-Sydney College, Hampden-Sydney, VA, USA.
Zachary C HandHargadon Laboratory, Department of Biology, Hampden-Sydney College, Hampden-Sydney, VA, USA.
Yonathan T ArarsoHargadon Laboratory, Department of Biology, Hampden-Sydney College, Hampden-Sydney, VA, USA.
Osric A ForrestHargadon Laboratory, Department of Biology, Hampden-Sydney College, Hampden-Sydney, VA, USA.
Hampden–Sydney College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic cells (DCs) are key regulators of host immunity that are capable of inducing either immune tolerance or activation. In addition to their well-characterized role in shaping immune responses to foreign pathogens, DCs are also known to be critical for the induction and maintenance of anti-tumor immune responses. Therefore, it is important to understand how tumors influence the function of DCs and the quality of immune responses they elicit. Although the majority of studies in this field to date have utilized either immortalized DC lines or DC populations that have been generated under artificial conditions from hematopoietic precursors in vitro, we wished to investigate how tumors impact the function of already differentiated, tissue-resident DCs. Therefore, we used both an ex vivo and in vivo model system to assess the influence of melanoma-derived factors on DC maturation and activation. In ex vivo studies with freshly isolated splenic DCs, we demonstrate that the extent to which DC maturation and activation are altered by these factors correlates with melanoma tumorigenicity, and we identify partial roles for tumor-derived transforming growth factor (TGF)β1 and vascular endothelial growth factor (VEGF)-A in the altered functionality of DCs. In vivo studies using a lung metastasis model of melanoma also demonstrate tumorigenicity-dependent alterations to the function of lung-resident DCs, and skewed production of proinflammatory cytokines and chemokines by these tumor-altered cells is associated with recruitment of an immune infiltrate that may ultimately favor tumor immune escape and outgrowth.

Indexed as

Cell DifferentiationAnimalsCD8-Positive T-LymphocytesCell CountChemokinesDendritic CellsGene Expression Regulation, NeoplasticGene Knockdown TechniquesImmunologic FactorsLungLymphocyte ActivationMacrophagesMelanoma, ExperimentalMice, Inbred C57BLSpleenTransforming Growth Factor beta1ChemokinesImmunologic FactorsTransforming Growth Factor beta1Vascular Endothelial Growth Factor A

Identifiers

PMID26010746
OpenAlexW410947787

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.