Evidence map›Paper›PMID 27364554›Full record

ArticleCancer research2016

BAFF and APRIL from Activin A-Treated Dendritic Cells Upregulate the Antitumor Efficacy of Dendritic Cells In Vivo.

Michael R Shurin, Yang Ma, Anton A Keskinov, Ruijing Zhao, Anna Lokshin, Marianna Agassandian, Galina V Shurin

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  9. Heliyon · 2023
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  15. Review
  16. Activin-A impedes the establishment of CD4Journal of experimental & clinical cancer research : CR · 2021
    Article
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  18. 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

7 authors at 2 institutions in 2 countries.

Michael R ShurinDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Yang MaDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Anton A KeskinovDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Ruijing ZhaoDepartment of Immunology, Hebei Medical University, Shijiazhuang, Hebei, China.
Anna LokshinDepartment of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Marianna AgassandianDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Galina V ShurinDepartment of Pathology, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania. shuringv@upmc.edu.
University of Pittsburgh Medical Center · USHebei Medical University · CN

Funding

Chemomodulation of the Tumor MicroenvironmentR01CA154369 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI SHURIN, MICHAEL R · 2011 to 2015
$1.5M
NCI NIH HHS R01 CA154369
6 · The paper itself

Abstract

The members of the TGFβ superfamily play a key role in regulating developmental and homeostasis programs by controlling differentiation, proliferation, polarization, and survival of different cell types. Although the role of TGFβ1 in inflammation and immunity is well evident, the contribution of other TGFβ family cytokines in the modulation of the antitumor immune response remains less documented. Here we show that activin A triggers SMAD2 and ERK1/2 pathways in dendritic cells (DC) expressing type I and II activin receptors, and upregulates production of the TNFα family cytokines BAFF (TALL-1, TNFSF13B) and APRIL (TALL-2, TNFSF13A), which is blocked by SMAD2 and ERK1/2 inhibitors, respectively. BAFF and APRIL derived from activin A-treated DCs upregulate proliferation and survival of T cells expressing the corresponding receptors, BAFF-R and TACI. In vivo, activin A-stimulated DCs demonstrate a significantly increased ability to induce tumor-specific CTLs and inhibit the growth of melanoma and lung carcinoma, which relies on DC-derived BAFF and APRIL, as knockdown of the BAFF and APRIL gene expression in activin A-treated DCs blocks augmentation of their antitumor potential. Although systemic administration of activin A, BAFF, or APRIL for the therapeutic purposes is not likely due to the pluripotent effects on malignant and nonmalignant cells, our data open a novel opportunity for improving the efficacy of DC vaccines. In fact, a significant augmentation of the antitumor activity of DC pretreated with activin A and the proven role of DC-derived BAFF and APRIL in the induction of antitumor immunity in vivo support this direction. Cancer Res; 76(17); 4959-69. ©2016 AACR.

Indexed as

ActivinsAnimalsB-Cell Activating FactorBlotting, WesternDendritic CellsFlow CytometryImmunophenotypingLymphocyte ActivationMaleMiceMice, Inbred C57BLNeoplasms, ExperimentalReverse Transcriptase Polymerase Chain ReactionT-LymphocytesTumor Necrosis Factor Ligand Superfamily Member 13Up-Regulationactivin AActivinsB-Cell Activating FactorTnfsf13b protein, mouseTnfsf13 protein, mouseTumor Necrosis Factor Ligand Superfamily Member 13

Identifiers

PMID27364554
PMCPMC5010463
OpenAlexW2464900585

What OpenQuestion holds

Textmetadata
LicenceTDM
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.