Evidence map›Paper›PMID 32023844›Full record

ArticleCells2020

Interleukin-6 Derived from the Central Nervous System May Influence the Pathogenesis of Experimental Autoimmune Encephalomyelitis in a Cell-Dependent Manner.

Paula Sanchis, Olaya Fernández-Gayol, Gemma Comes, Anna Escrig, Mercedes Giralt, Richard D Palmiter, Juan Hidalgo

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. 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
2.6field-weighted citation impact, top 10% 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, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. A suitable model to investigate acute neurological consequences of coronavirus infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  6. Bystander activation of microglia byFrontiers in immunology · 2023
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. 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

7 authors at 2 institutions in 2 countries.

Paula SanchisInstitute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Olaya Fernández-GayolInstitute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Gemma ComesInstitute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Anna EscrigInstitute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Mercedes GiraltInstitute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Richard D PalmiterDepartment of Biochemistry, Genome Sciences, and Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.
Juan HidalgoInstitute of Neurosciences and Department of Cellular Biology, Physiology and Immunology, Faculty of Biosciences, Universitat Autònoma de Barcelona, 08193 Barcelona, Spain.
Universitat Autònoma de Barcelona · ESHoward Hughes Medical Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInterleukin-6 (IL-6) is a pleiotropic and multifunctional cytokine that plays a critical role in induction of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). Although EAE has always been considered a peripherally elicited disease, Il6 expression exclusively within central nervous system is sufficient to induce EAE development. Neurons, astrocytes, and microglia can secrete and respond to IL-6.

methodsTo dissect the relevance of each cell source for establishing EAE, we generated and immunized conditional Il6 knockout mice for each of these cell types with myelin oligodendrocyte glycoprotein 35-55 (MOG RESULTS AND

conclusionsThe combined results reveal a minor role for Il6 expression in both astrocytes and microglia for symptomatology and neuropathology of EAE, whereas neuronal Il6 expression was not relevant for the variables analyzed.

Indexed as

AnimalsCentral Nervous SystemCX3C Chemokine Receptor 1Demyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalFemaleGene Expression RegulationGlial Fibrillary Acidic ProteinGliosisInflammationInterleukin-6MaleMice, Inbred C57BLMice, KnockoutMyelin-Oligodendrocyte GlycoproteinSpinal CordCX3C Chemokine Receptor 1Cx3cr1 protein, mouseGlial Fibrillary Acidic ProteinInterleukin-6Myelin-Oligodendrocyte Glycoproteinconditional IL-6 knockoutexperimental autoimmune encephalomyelitisMOG35-55peptideneuroinflammation

Identifiers

PMID32023844
PMCPMC7072597
OpenAlexW3003849319

What OpenQuestion holds

Textmetadata
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.