ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Suppressor of cytokine signaling 1 expression protects oligodendrocytes from the deleterious effects of interferon-gamma.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 58 citations in OpenAlex.
- Mechanistic insights and therapeutic potential of targeting the cGAS-STING pathway in neurodegenerative diseases.Journal of neuroinflammation · 2026Review
- Cerebellar hypomyelination, white matter vacuolization, and prolonged presence of atypical porcine pestivirus in pigs with congenital tremor type A-II.Veterinary pathology · 2026Article
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
- Heparanome-Mediated Rescue of Oligodendrocyte Progenitor Quiescence following Inflammatory Demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- hsa-MiR-19a-3p and hsa-MiR-19b-3p Are Associated with Spinal Cord Injury-Induced Neuropathic Pain: Findings from a Genome-Wide MicroRNA Expression Profiling Screen.Neurotrauma reports · 2021Article
- The control of oligodendrocyte bioenergetics by interferon-gamma (IFN-γ) and Src homology region 2 domain-containing phosphatase-1 (SHP-1).Journal of neuroimmunology · 2019Article
- Increase in chemokine CXCL1 by ERβ ligand treatment is a key mediator in promoting axon myelination.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Article
- Regulation of Macrophage, Dendritic Cell, and Microglial Phenotype and Function by the SOCS Proteins.Frontiers in immunology · 2015Review
- Opportunities for Translation from the Bench: Therapeutic Intervention of the JAK/STAT Pathway in Neuroinflammatory Diseases.Critical reviews in immunology · 2015Review
- Promoting remyelination: utilizing a viral model of demyelination to assess cell-based therapies.Expert review of neurotherapeutics · 2014Review
- AMP-activated protein kinase signaling protects oligodendrocytes that restore central nervous system functions in an experimental autoimmune encephalomyelitis model.The American journal of pathology · 2013Article
- Oligodendrocyte-specific activation of PERK signaling protects mice against experimental autoimmune encephalomyelitis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- CXCR2 signaling and host defense following coronavirus-induced encephalomyelitis.Future virology · 2012Article
- Molecular mechanisms of oligodendrocyte injury in multiple sclerosis and experimental autoimmune encephalomyelitis.International journal of molecular sciences · 2012Review
- CXCR2 signaling protects oligodendrocyte progenitor cells from IFN-γ/CXCL10-mediated apoptosis.Glia · 2011Article
- Overexpression of the dominant-negative form of interferon regulatory factor 1 in oligodendrocytes protects against experimental autoimmune encephalomyelitis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Cooperative contributions of interferon regulatory factor 1 (IRF1) and IRF8 to interferon-γ-mediated cytotoxic effects on oligodendroglial progenitor cells.Journal of neuroinflammation · 2011Article
- Transgenic models for cytokine-induced neurological disease.Biochimica et biophysica acta · 2010Review
- Interferon-γ inhibits central nervous system myelination through both STAT1-dependent and STAT1-independent pathways.Journal of neuroscience research · 2010Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Interferon-gamma (IFN-gamma) is a pleiotropic cytokine produced by T cells and natural killer cells that has been implicated as a deleterious factor in the immune-mediated demyelinating disorder multiple sclerosis. In vitro, purified developing and mature oligodendrocytes have been shown to die in the presence of IFN-gamma by apoptosis and necrosis, respectively. Moreover, transgenic expression of IFN-gamma in the CNS of mice during development results in tremor, hypomyelination, and oligodendrocyte cell loss, and IFN-gamma expression in adult animals after demyelinating insults inhibits remyelination. To examine the molecular mechanisms of IFN-gamma-induced oligodendrocyte injury, we generated a transgenic mouse line [PLP/SOCS1 (proteolipid protein/suppressor of cytokine signaling 1)] that exhibits diminished oligodendrocyte responsiveness to IFN-gamma attributable to the targeted expression of SOCS1 in these cells. We demonstrate that oligodendrocytes in the PLP/SOCS1 transgenic mice are protected against the injurious effect of IFN-gamma. Our data indicate that IFN-gamma exerts a direct deleterious effect on developing oligodendrocytes. The capacity of SOCS1 to inhibit the effects of IFN-gamma suggests a therapeutic approach toward protection of myelinating oligodendrocytes against the harmful effects of inflammation.
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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.