Evidence map›Paper›PMID 41808190›Full record

ArticleJournal of neuroinflammation2026

Enhanced myelination potential of human mature oligodendrocytes by TNF and IFNG combination.

Abdulshakour Mohammadnia, Qiao-Ling Cui, Moein Yaqubi, Gabriela J Blaszczyk, Chao Weng, Jeffery A Hall, Roy Dudley, Jo Anne Stratton, Stephanie Zandee, Timothy E Kennedy and 2 more

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Abdulshakour Mohammadnia *Department of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Qiao-Ling Cui *Department of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Moein YaqubiDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Gabriela J BlaszczykDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Chao WengDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Jeffery A HallDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Roy DudleyDepartment of Pediatric Neurosurgery, Montreal Children's Hospital, Montreal, H4A 3J1, Canada.
Jo Anne StrattonDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Stephanie ZandeeDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Timothy E KennedyDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada.
Myriam SrourDivision of Pediatric Neurology, Montreal Children's Hospital, Montreal, H4A 3J1, Canada.
Jack P AntelDepartment of Neurology and Neurosurgery, Neuroimmunology Unit, Montreal Neurological Institute, McGill University, 3801 Rue University, Montréal, QC, H3A 2B4, Canada. jack.antel@mcgill.ca.

Funding

International Progressive MS Alliance PA-1604-08492
6 · The paper itself

Abstract

Initial phases of multiple sclerosis (MS) are characterized by recurrent focal inflammation within the central nervous system associated with demyelination and variable subsequent remyelination, indicating that both injury and repair are ongoing within the same microenvironment. An array of pro-inflammatory molecules including tumor necrosis factor α (TNF) and interferon γ (IFNG) are implicated as contributing to oligodendrocyte (OL) lineage cell injury in MS and its models. Using OL lineage cells derived from human surgical samples, we observed that TNF and IFNG in combination enhanced ensheathment of synthetic nanofibers by mature OLs compared to those observed under control conditions or in the presence of individual cytokines, reaching levels comparable to those of A2B5+ late-stage progenitor cells. The combination reversed the individual cytokine mediated inhibition of A2B5+ cell ensheathment. Molecular analysis of the mature OL population identified increased expression of myelination relevant genes in the cytokine combination treated cells, of STAT and IRF transcription factors (TFs) that regulate many of these genes, and of mature OL structural genes (MOBP and CNP). TNF and IFNG combination also reduced expression of OPC signature genes in the mature OLs compared to IFNG alone. The combination effect on ensheathment was reversed using a JAK/STAT pathway inhibitor. The combination of TNF and IFNG induced a stronger immune signature in mature OLs compared to individual cytokines. These results emphasize the complex positive and negative interplay of inflammatory responses in the CNS and the potential for therapeutic modulation.

Indexed as

Interferon-gammaMyelin SheathOligodendrogliaTumor Necrosis Factor-alphaCell DifferentiationCells, CulturedHumansInterferon-gammaTumor Necrosis Factor-alpha

Identifiers

PMID41808190
PMCPMC13088765

What OpenQuestion holds

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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.