Evidence map›Paper›PMID 28861085›Full record

ArticleFrontiers in immunology2017

Neurotrophin Receptor p75NTR Regulates Immune Function of Plasmacytoid Dendritic Cells.

Joanna Bandoła, Cornelia Richter, Martin Ryser, Arshad Jamal, Michelle P Ashton, Malte von Bonin, Matthias Kuhn, Benjamin Dorschner, Dimitra Alexopoulou, Katrin Navratiel and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. 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 35% 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, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. P75iScience · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Deletion of p75Frontiers in molecular neuroscience · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Up-regulation of proBDNF/p75Science advances · 2022
    Article
  14. Article
  15. Article
  16. Plasmacytoid dendritic cells in the eye.Progress in retinal and eye research · 2021
    Review
  17. Article
  18. Article
  19. Article
  20. 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

16 authors at 3 institutions in 2 countries.

Joanna BandołaDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Cornelia RichterDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Martin RyserDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Arshad JamalDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Michelle P AshtonDFG-Center for Regenerative Therapies Dresden, Cluster of Excellence, Technische Universitaet Dresden, Dresden, Germany.
Malte von BoninMedical Clinic I, University Clinic Dresden, Dresden, Germany.
Matthias KuhnFaculty of Medicine, Institute for Medical Informatics and Biometry, Technische Universitaet Dresden, Dresden, Germany.
Benjamin DorschnerDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Dimitra AlexopoulouBIOTEChnology Center/DFG-Center for Regenerative Therapies Dresden, Cluster of Excellence, Technische Universitaet Dresden, Dresden, Germany.
Katrin NavratielDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Ingo RoederFaculty of Medicine, Institute for Medical Informatics and Biometry, Technische Universitaet Dresden, Dresden, Germany.
Andreas DahlBIOTEChnology Center/DFG-Center for Regenerative Therapies Dresden, Cluster of Excellence, Technische Universitaet Dresden, Dresden, Germany.
Christian M HedrichDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Ezio BonifacioDFG-Center for Regenerative Therapies Dresden, Cluster of Excellence, Technische Universitaet Dresden, Dresden, Germany.
Sebastian BrennerDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Sebastian ThiemeDepartment of Pediatrics, University Clinic Dresden, Dresden, Germany.
Technische Universität Dresden · DEDeutschen Konsortium für Translationale Krebsforschung · DEImperial College of Business Studies · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) regulate innate and adaptive immunity. Neurotrophins and their receptors control the function of neuronal tissue. In addition, they have been demonstrated to be part of the immune response but little is known about the effector immune cells involved. We report, for the first time, the expression and immune-regulatory function of the low affinity neurotrophin receptor p75 neurotrophin receptor (p75NTR) by the antigen-presenting pDCs, mediated by toll-like receptor (TLR) 9 activation and differential phosphorylation of interferon regulatory factor 3 and 7. The modulation of p75NTR on pDCs significantly influences disease progression of asthma in an ovalbumin-induced mouse model mediated by the TLR9 signaling pathway. p75NTR activation of pDCs from patients with asthma increased allergen-specific T cell proliferation and cytokine secretion in nerve growth factor concentration-dependent manner. Further, p75NTR activation of pDCs delayed the onset of autoimmune diabetes in RIP-CD80GP mice and aggravated graft-versus-host disease in a xenotransplantation model. Thus, p75NTR signaling on pDCs constitutes a new and critical mechanism connecting neurotrophin signaling and immune response regulation with great therapeutic potential for a variety of immune disorders.

Indexed as

allergic asthmaautoimmune diabetesgraft-versus-host diseaseneurotrophinp75 neurotrophin receptorplasmacytoid dendritic cellsTLR9

Identifiers

PMID28861085
PMCPMC5562693
OpenAlexW2748585716

What OpenQuestion holds

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LicenceCC BY
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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.