Evidence map›Paper›PMID 39040539›Full record

ArticleFrontiers in neurology2024

Advancing understanding of the role of IL-22 in myelination: insights from the Cuprizone mouse model.

Imen Zamali, Ines Elbini, Raja Rekik, Nour-Elhouda Neili, Wafa Ben Hamouda, Ahlem Ben Hmid, Raoudha Doghri, Mélika Ben Ahmed

Abstract read
In one paragraph

Article in Frontiers in neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Fisetin Mitigates Ferroptosis and Promotes Remyelination in a Cuprizone Model of Multiple Sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    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

8 authors.

Imen ZamaliLaboratory of Transmission, Control and Immunobiology of Infection, Institut Pasteur de Tunis, Tunis, Tunisia.
Ines ElbiniLaboratory of Biomolecules, Venoms and Theranostic Applications (LR20IPT01), Pasteur Institute of Tunis, University of Tunis El Manar, Tunis, Tunisia.
Raja RekikLaboratory of Transmission, Control and Immunobiology of Infection, Institut Pasteur de Tunis, Tunis, Tunisia.
Nour-Elhouda NeiliLaboratory of Biomolecules, Venoms and Theranostic Applications (LR20IPT01), Pasteur Institute of Tunis, University of Tunis El Manar, Tunis, Tunisia.
Wafa Ben HamoudaLaboratory of Transmission, Control and Immunobiology of Infection, Institut Pasteur de Tunis, Tunis, Tunisia.
Ahlem Ben HmidLaboratory of Transmission, Control and Immunobiology of Infection, Institut Pasteur de Tunis, Tunis, Tunisia.
Raoudha DoghriFaculté de Médecine de Tunis, University of Tunis El Manar, Tunis, Tunisia.
Mélika Ben AhmedLaboratory of Transmission, Control and Immunobiology of Infection, Institut Pasteur de Tunis, Tunis, Tunisia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite significant advancements in the field, the pathophysiology of multiple sclerosis (MS) remains partially understood, with limited therapeutic options available for this debilitating condition. The precise impact of Interleukin-22 (IL-22) in the context of MS is still incompletely elucidated with some evidence suggesting its protective role. To provide a more comprehensive understanding of the role of IL-22, we investigated its effect on remyelination in a mouse model of demyelination induced by Cuprizone. Mice underwent a 6 week regimen of Cuprizone or vehicle, followed or not by intraperitoneal administration of IL-22. Behavioral assessments including tail suspension and inverted screen tests were conducted, alongside histological, histochemical, and quantitative PCR analyses. In Cuprizone-treated mice, IL-22 significantly improved motor and behavioral performance and robustly promoted remyelination in the

Indexed as

Cuprizone mouse modelIL-22multiple sclerosismyelinationmyelin basic protein

Identifiers

PMID39040539
PMCPMC11260746

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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.