Evidence map›Paper›PMID 28331179›Full record

ArticleScientific reports2017

Hyperosmolarity impedes the cross-priming competence of dendritic cells in a TRIF-dependent manner.

Zoran V Popovic, Maria Embgenbroich, Federica Chessa, Viola Nordström, Mahnaz Bonrouhi, Thomas Hielscher, Norbert Gretz, Shijun Wang, Daniel Mathow, Thomas Quast and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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  6. Review
  7. Review
  8. Article
  9. Interplay of NaFrontiers in immunology · 2019
    Review
  10. Review
  11. Article
  12. Salt, Hypertension, and Immunity.Annual review of physiology · 2018
    Review
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

14 authors at 3 institutions in 1 country.

Zoran V PopovicDepartment of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany. z.popovic@dkfz.de.
Maria EmbgenbroichDepartment of Cellular Immunology, LIMES Institute, University of Bonn, Bonn, Germany.
Federica ChessaDepartment of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany.
Viola NordströmDepartment of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany.
Mahnaz BonrouhiDepartment of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany.
Thomas HielscherDepartment of Biostatistics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0003-1277-310X
Norbert GretzMedical Research Center, University Hospital Mannheim, University of Heidelberg, Mannheim, Germany.
Shijun WangDepartment of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany.
Daniel MathowDepartment of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany.
Thomas QuastDepartment of Molecular Immunology and Cell Biology, LIMES Institute, University of Bonn, Bonn, Germany.
Jan-Gero SchloetelDepartment of Membrane Biochemistry, LIMES Institute, University of Bonn, Bonn, Germany.
Waldemar KolanusDepartment of Molecular Immunology and Cell Biology, LIMES Institute, University of Bonn, Bonn, Germany.
Sven BurgdorfDepartment of Cellular Immunology, LIMES Institute, University of Bonn, Bonn, Germany.
Hermann-Josef GröneDepartment of Cellular and Molecular Pathology, German Cancer Research Center, Heidelberg, Germany. h.-j.groene@dkfz.de.
German Cancer Research Center · DEUniversity of Bonn · DEHeidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tissue osmolarity varies among different organs and can be considerably increased under pathologic conditions. Hyperosmolarity has been associated with altered stimulatory properties of immune cells, especially macrophages and dendritic cells. We have recently reported that dendritic cells upon exposure to hypertonic stimuli shift their profile towards a macrophage-M2-like phenotype, resulting in attenuated local alloreactivity during acute kidney graft rejection. Here, we examined how hyperosmotic microenvironment affects the cross-priming capacity of dendritic cells. Using ovalbumin as model antigen, we showed that exposure of dendritic cells to hyperosmolarity strongly inhibits activation of antigen-specific T cells despite enhancement of antigen uptake, processing and presentation. We identified TRIF as key mediator of this phenomenon. Moreover, we detected a hyperosmolarity-triggered, TRIF-dependent clustering of MHCI loaded with the ovalbumin-derived epitope, but not of overall MHCI molecules, providing a possible explanation for a reduced T cell activation. Our findings identify dendritic cells as important players in hyperosmolarity-mediated immune imbalance and provide evidence for a novel pathway of inhibition of antigen specific CD8

Indexed as

Cross-PrimingOsmotic PressureAdaptor Proteins, Vesicular TransportAnimalsAntigensCD8-Positive T-LymphocytesCells, CulturedDendritic CellsHistocompatibility Antigens Class IMice, Inbred C57BLOvalbuminAdaptor Proteins, Vesicular TransportAntigensHistocompatibility Antigens Class IOvalbuminTicam1 protein, mouse

Identifiers

PMID28331179
PMCPMC5428499
OpenAlexW2597297943

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.