Evidence map›Paper›PMID 21703422›Full record

ArticleThe American journal of pathology2011

Human renal cell carcinoma induces a dendritic cell subset that uses T-cell crosstalk for tumor-permissive milieu alterations.

Ainhoa-M Figel, Dorothee Brech, Petra U Prinz, Ulrike K Lettenmeyer, Judith Eckl, Adriana Turqueti-Neves, Josef Mysliwietz, David Anz, Nicole Rieth, Niklas Muenchmeier and 6 more

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.2field-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

28 citing papers in PubMed, 46 citations in OpenAlex.

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  12. Impact of anatomic site on antigen-presenting cells in cancer.Journal for immunotherapy of cancer · 2020
    Review
  13. Article
  14. Review
  15. Implications of the tumor immune microenvironment for staging and therapeutics.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2018
    Review
  16. Article
  17. Article
  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

16 authors at 6 institutions in 3 countries.

Ainhoa-M FigelInstitute of Molecular Immunology, Helmholtz Zentrum München, German Research Center for Environmental Health, Munich, Germany.
Dorothee Brech
Petra U Prinz
Ulrike K Lettenmeyer
Judith Eckl
Adriana Turqueti-Neves
Josef Mysliwietz
David Anz
Nicole Rieth
Niklas Muenchmeier
Alexander Buchner
Stefan Porubsky
Sabine I Siegert
Stephan Segerer
Peter J Nelson
Elfriede Noessner
Center for Environmental Health · USPolyclinic Medical University · CHGerman Cancer Research Center · DEHelmholtz Zentrum München · DELudwig-Maximilians-Universität München · DEUniversity of Zurich · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue dendritic cells (DCs) may influence the progression of renal cell carcinoma (RCC) by regulating the functional capacity of antitumor effector cells. DCs and their interaction with T cells were analyzed in human RCC and control kidney tissues. The frequency of CD209(+) DCs in RCCs was found to be associated with an unfavorable T(H)1 cell balance in the tissue and advanced tumor stages. The CD209(+) DCs in RCC were unusual because most of them co-expressed macrophage markers (CD14, CD163). The phenotype of these enriched-in-renal-carcinoma DCs (ercDCs) could be reiterated in vitro by carcinoma-secreted factors (CXCL8/IL-8, IL-6, and vascular endothelial growth factor). ErcDCs resembled conventional DCs in costimulatory molecule expression and antigen cross-presentation. They did not suppress cognate cytotoxic T-lymphocyte function and did not cause CD3ζ down-regulation, FOXP3 induction, or T-cell apoptosis in situ or in vitro; thus, they are different from classic myeloid-derived suppressor cells. ErcDCs secreted high levels of metalloproteinase 9 and used T-cell crosstalk to increase tumor-promoting tumor necrosis factor α and reduce chemokines relevant for T(H)1-polarized lymphocyte recruitment. This modulation of the tumor environment exerted by ercDCs suggests an immunologic mechanism by which tumor control can fail without involving cytotoxic T-lymphocyte inhibition. Pharmacologic targeting of the deviated DC differentiation could improve the efficacy of immunotherapy against RCC.

Indexed as

AdultAgedAged, 80 and overApoptosisBlotting, WesternCarcinoma, Renal CellCase-Control StudiesCell DifferentiationCell MovementCell ProliferationChemokinesCross-PrimingCytokinesDendritic CellsEndocytosisFemaleChemokinesCytokinesInterleukin-6RNA, Messenger

Identifiers

PMID21703422
PMCPMC3123875
OpenAlexW2027554407

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.