Evidence map›Paper›PMID 28084589›Full record

ArticleMolecular neurobiology2018

IL-17A Promotes Granulocyte Infiltration, Myelin Loss, Microglia Activation, and Behavioral Deficits During Cuprizone-Induced Demyelination.

Julian Zimmermann, Michael Emrich, Marius Krauthausen, Simon Saxe, Louisa Nitsch, Michael T Heneka, Iain L Campbell, Marcus Müller

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2018. 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
2.0field-weighted citation impact, top 14% 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, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Genes in Axonal Regeneration.Molecular neurobiology · 2024
    Review
  5. Article
  6. Article
  7. Astrocytes: Lessons Learned from the Cuprizone Model.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
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  15. 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

8 authors at 2 institutions in 2 countries.

Julian ZimmermannDepartment of Neurology, University of Bonn, Sigmund-Freud-Str 25, 53127, Bonn, Germany. julian.zimmermann@ukb.uni-bonn.de.ORCID 0000-0003-1964-0078
Michael EmrichDepartment of Neurology, University of Bonn, Sigmund-Freud-Str 25, 53127, Bonn, Germany.
Marius KrauthausenDepartment of Neurology, University of Bonn, Sigmund-Freud-Str 25, 53127, Bonn, Germany.
Simon SaxeDepartment of Neurology, University of Bonn, Sigmund-Freud-Str 25, 53127, Bonn, Germany.
Louisa NitschDepartment of Neurology, University of Bonn, Sigmund-Freud-Str 25, 53127, Bonn, Germany.
Michael T HenekaClinical Neurosciences, Department of Neurology, University of Bonn, Bonn, Germany.
Iain L CampbellSchool of Molecular Bioscience, University of Sydney, Sydney, NSW, Australia.
Marcus MüllerDepartment of Neurology, University of Bonn, Sigmund-Freud-Str 25, 53127, Bonn, Germany.
University of Bonn · DEThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent evidence suggests a pivotal role of the proinflammatory cytokine interleukin - 17A (IL-17) in demyelinating autoimmune diseases of the central nervous system (CNS) such as multiple sclerosis (MS). Nevertheless, it remains unclear if this cytokine exerts direct effects on CNS resident cells during MS or modulates the function of infiltrating immune cells towards a more detrimental phenotype. Here, we investigated the effects of locally produced IL-17 during experimental demyelination of the CNS using the cuprizone (CPZ) model in mice with (GF/IL17) or without transgenic production of IL-17 by astrocytes in the CNS. During early demyelination, GF/IL17 mice demonstrated enhanced activity and decreased anxiety-related behavior in the elevated plus maze suggesting a more severe disease course. Furthermore, in GF/IL17 mice, toxic demyelination was accelerated and synthesis of myelin proteins was reduced. Early demyelination was accompanied by an increased ratio of infiltrating granulocytes in GF/ILl17 mice. The presence of IL-17 during CPZ treatment increased the accumulation of activated microglia and sustained microglial proliferation during myelin loss. Taken together, our results argue for a detrimental role of IL-17 during demyelinating diseases.

Indexed as

AnimalsAnxietyAstrocytesBehavior, AnimalCell ProliferationCuprizoneDemyelinating DiseasesDisease Models, AnimalGranulocytesInterleukin-17MiceMice, TransgenicMicrogliaMyelin SheathCuprizoneInterleukin-17CuprizoneCytokinesDemyelinationGranulocytesInterleukin-17Myelin

Identifiers

PMID28084589
OpenAlexW2576020905

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.