Evidence map›Paper›PMID 26612827›Full record

ArticleThe EMBO journal2016

Gatekeeper role of brain antigen-presenting CD11c+ cells in neuroinflammation.

Magdalena Paterka, Volker Siffrin, Jan O Voss, Johannes Werr, Nicola Hoppmann, René Gollan, Patrick Belikan, Julia Bruttger, Jérôme Birkenstock, Steffen Jung and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Review
  3. An IL-23-STAT4 pathway is required for the proinflammatory function of classical dendritic cells during CNS inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Review
  5. Article
  6. Autophagy pathways in autoimmune diseases.Journal of autoimmunity · 2023
    Review
  7. 1,2-Current issues in molecular biology · 2023
    Article
  8. Contribution of Intravital Neuroimaging to Study Animal Models of Multiple Sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. CD11cFrontiers in immunology · 2019
    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

15 authors at 6 institutions in 3 countries.

Magdalena PaterkaDepartment of Neurology, Focus Program Translational Neurosciences (FTN), Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn²) University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Volker SiffrinDepartment of Neurology, Focus Program Translational Neurosciences (FTN), Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn²) University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Jan O VossMolecular Neurology, Max Delbrück Center for Molecular Medicine Berlin-Buch, Berlin, Germany.
Johannes WerrMolecular Neurology, Max Delbrück Center for Molecular Medicine Berlin-Buch, Berlin, Germany.
Nicola HoppmannDepartment of Neurology, Focus Program Translational Neurosciences (FTN), Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn²) University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
René GollanDepartment of Neurology, Focus Program Translational Neurosciences (FTN), Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn²) University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Patrick BelikanDepartment of Neurology, Focus Program Translational Neurosciences (FTN), Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn²) University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Julia BruttgerInstitute for Molecular Medicine, Research Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Jérôme BirkenstockDepartment of Neurology, Focus Program Translational Neurosciences (FTN), Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn²) University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Steffen JungDepartment of Immunology Weizmann Institute of Science, Rehovot, Israel.
Enric EspluguesHoward Hughes Medical Institute Yale University School of Medicine, New Haven, CT, USA.
Nir YogevInstitute for Molecular Medicine, Research Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University Mainz, Mainz, Germany.
Richard A FlavellHoward Hughes Medical Institute Yale University School of Medicine, New Haven, CT, USA.
Tobias BoppInstitute for Immunology, Research Center for Immunotherapy (FZI), University Medical Center of the Johannes Gutenberg University, Mainz, Germany.
Frauke ZippDepartment of Neurology, Focus Program Translational Neurosciences (FTN), Research Center for Immunotherapy (FZI), Rhine-Main Neuroscience Network (rmn²) University Medical Center of the Johannes Gutenberg University, Mainz, Germany frauke.zipp@unimedizin-mainz.de.
University Medical Center of the Johannes Gutenberg University Mainz · DEJohannes Gutenberg University Mainz · DEMax Delbrück Center · DEHoward Hughes Medical Institute · USWeizmann Institute of Science · ILYale University · US

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI DAVID L RIMM · 1985 to 2026
$85.0M
NCI NIH HHS P30 CA016359
6 · The paper itself

Abstract

Multiple sclerosis is the most frequent chronic inflammatory disease of the CNS. The entry and survival of pathogenic T cells in the CNS are crucial for the initiation and persistence of autoimmune neuroinflammation. In this respect, contradictory evidence exists on the role of the most potent type of antigen-presenting cells, dendritic cells. Applying intravital two-photon microscopy, we demonstrate the gatekeeper function of CNS professional antigen-presenting CD11c(+) cells, which preferentially interact with Th17 cells. IL-17 expression correlates with expression of GM-CSF by T cells and with accumulation of CNS CD11c(+) cells. These CD11c(+) cells are organized in perivascular clusters, targeted by T cells, and strongly express the inflammatory chemokines Ccl5, Cxcl9, and Cxcl10. Our findings demonstrate a fundamental role of CNS CD11c(+) cells in the attraction of pathogenic T cells into and their survival within the CNS. Depletion of CD11c(+) cells markedly reduced disease severity due to impaired enrichment of pathogenic T cells within the CNS.

Indexed as

AnimalsAntigen-Presenting CellsBrainCD11c AntigenCell MovementDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-17Mice, Inbred C57BLTh17 CellsT-LymphocytesCD11c AntigenGranulocyte-Macrophage Colony-Stimulating FactorInterleukin-17chemokinesdendritic cellsEAE/MSTh17two‐photon microscopy

Identifiers

PMID26612827
PMCPMC4718005
OpenAlexW2187274112

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.