ArticleJournal of neuroscience research2010
Interferon-γ inhibits central nervous system myelination through both STAT1-dependent and STAT1-independent pathways.
Article in Journal of neuroscience research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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.
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.
Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
- The key role of the ferroptosis mechanism in neurological diseases and prospects for targeted therapy.Frontiers in neuroscience · 2025Review
- Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.Cells · 2024Review
- Beneficial Effects of Plant Oils Supplementation on Multiple Sclerosis: A Comprehensive Review of Clinical and Experimental Studies.Nutrients · 2023Review
- An early glycolysis burst in microglia regulates mitochondrial dysfunction in oligodendrocytes under neuroinflammation.iScience · 2023Article
- The transcription factor Stat-1 is essential for Schwann cell differentiation, myelination and myelin sheath regeneration.Molecular medicine (Cambridge, Mass.) · 2023Article
- Autoreactive lymphocytes in multiple sclerosis: Pathogenesis and treatment target.Frontiers in immunology · 2022Review
- Detection of PERK Signaling in the Central Nervous System.Methods in molecular biology (Clifton, N.J.) · 2022Article
- The differentiation state of the Schwann cell progenitor drives phenotypic variation between two contagious cancers.PLoS pathogens · 2021Article
- Endoplasmic Reticulum Stress-Associated Neuronal Death and Innate Immune Response in Neurological Diseases.Frontiers in immunology · 2021Review
- Microglia Impede Oligodendrocyte Generation in Aged Brain.Journal of inflammation research · 2021Article
- Extrinsic immune cell-derived, but not intrinsic oligodendroglial factors contribute to oligodendroglial differentiation block in multiple sclerosis.Acta neuropathologica · 2020Article
- Unfolded protein response in myelin disorders.Neural regeneration research · 2020Review
- iPSCs from people with MS can differentiate into oligodendrocytes in a homeostatic but not an inflammatory milieu.PloS one · 2020Article
- Melatonin and Multiple Sclerosis: From Plausible Neuropharmacological Mechanisms of Action to Experimental and Clinical Evidence.Clinical drug investigation · 2019Review
- Inhibitory Effect of LPS on the Proliferation of Oligodendrocyte Precursor Cells through the Notch Signaling Pathway in Intrauterine Infection-induced Rats.Current medical science · 2018Article
- Role of nuclear factor κB in multiple sclerosis and experimental autoimmune encephalomyelitis.Neural regeneration research · 2018Review
- Article
- Maternal Overnutrition Programs Central Inflammation and Addiction-Like Behavior in Offspring.BioMed research international · 2018Review
- NF-κB Activation Protects Oligodendrocytes against Inflammation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The immune cytokine interferon-gamma (IFN-gamma) plays a crucial role in immune-mediated demyelinating diseases such as multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). Our previous studies have shown that enforced expression of IFN-gamma in the central nervous system (CNS) inhibits developmental myelination or remyelination in EAE demyelinated lesions. Although many of the cellular actions of IFN-gamma result from its activation of the signal transducer and activator of transcription 1 (STAT1) pathway, recent studies have shown that STAT1-independent pathways regulate some facets of IFN-gamma biology. In this study, we dissected the role ofSTAT1-dependent and STAT1-independent pathways in IFN-gamma-induced hypomyelination using a genetic approach. We found that the induction of STAT1-dependent, IFN-gamma-responsive genes in response to this cytokine was abolished in the CNS of STAT1 null mice. Moreover, STAT1 deletion diminished oligodendrocyte loss, reduction of myelinated axons, and the inflammatory response in the CNS of transgenic mice that ectopically expressed IFN-gamma in the CNS. Nevertheless, IFN-gamma-induced reduction of myelin sheath thickness in the CNS of these mice was not altered by STAT1 deletion. Collectively, these data demonstrate that both STAT1-dependent and STAT1-independent pathways are involved in the detrimental effects of IFN-gamma on the myelination process.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.