ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
IL-17-induced Act1-mediated signaling is critical for cuprizone-induced demyelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 78 citations in OpenAlex.
- Therapeutic Effects of Combined 6-Shogaol and Ibudilast on Neuroinflammation and Behavioral Deficits in a Cuprizone Mouse Model of Multiple Sclerosis.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Inhibition of Lin-11, Isl-1, and Mec‑3 Kinase (LIMK) Activity Attenuates Astrogliosis and Vascular Remodeling in an Experimental Model of Cuprizone-Induced Demyelination in Mice.ACS pharmacology & translational science · 2026Article
- Niraparib Demonstrates Therapeutic Potential in Multiple Sclerosis through Inhibition of IL-17A Receptor Interaction and Promotion of Remyelination.ACS chemical neuroscience · 2025Article
- Betaine alleviates deficits in motor behavior, neurotoxic effects, and neuroinflammatory responses in a rat model of demyelination.Toxicology reports · 2025Article
- Alpha-mangostin Ameliorates Apoptosis, Inflammation and Oxidative Stress in Cuprizone-induced Demyelination in C57BL/6 Mice.Basic and clinical neuroscience · 2025Article
- Glial Cells as Key Regulators in Neuroinflammatory Mechanisms Associated with Multiple Sclerosis.International journal of molecular sciences · 2024Review
- Astrocytes: Lessons Learned from the Cuprizone Model.International journal of molecular sciences · 2023Review
- FKBP5 activates mitophagy by ablating PPAR-γ to shape a benign remyelination environment.Cell death & disease · 2023Article
- Remyelination in animal models of multiple sclerosis: finding the elusive grail of regeneration.Frontiers in molecular neuroscience · 2023Review
- Reaction of different cell types of the brain on neurotoxin cuprizone and hormone melatonin treatment in young and aging mice.Frontiers in cellular neuroscience · 2023Article
- Oligodendrocyte death and myelin loss in the cuprizone model: an updated overview of the intrinsic and extrinsic causes of cuprizone demyelination.Molecular neurodegeneration · 2022Review
- TRPA1 Role in Inflammatory Disorders: What Is Known So Far?International journal of molecular sciences · 2022Review
- Mesenchymal Stem Cells Ameliorate Cuprizone-Induced Demyelination by Targeting Oxidative Stress and Mitochondrial Dysfunction.Cellular and molecular neurobiology · 2021Article
- Fundamentally different roles of neuronal TNF receptors in CNS pathology: TNFR1 and IKKβ promote microglial responses and tissue injury in demyelination while TNFR2 protects against excitotoxicity in mice.Journal of neuroinflammation · 2021Article
- STEAP4 expression in CNS resident cells promotes Th17 cell-induced autoimmune encephalomyelitis.Journal of neuroinflammation · 2021Article
- Repurposing of Secukinumab as Neuroprotective in Cuprizone-Induced Multiple Sclerosis Experimental Model via Inhibition of Oxidative, Inflammatory, and Neurodegenerative Signaling.Molecular neurobiology · 2020Article
- Loss of TMEM106B leads to myelination deficits: implications for frontotemporal dementia treatment strategies.Brain : a journal of neurology · 2020Article
- Temporal and Spatial Dynamics of Astroglial Reaction and Immune Response in Cuprizone-Induced Demyelination.Neurotoxicity research · 2020Article
- Dimethyl fumarate impairs differentiated B cells and fosters central nervous system integrity in treatment of multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2019Article
- Cuprizone toxicity andHeliyon · 2019Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Cuprizone inhibits mitochondrial function and induces demyelination in the corpus callosum, which resembles pattern III lesions in multiple sclerosis patients. However, the molecular and cellular mechanism by which cuprizone induces demyelination remains unclear. Interleukin-17 (IL-17) secreted by T helper 17 cells and γδT cells are essential in the development of experimental autoimmune encephalomyelitis. In this study, we examined the importance of IL-17 signaling in cuprizone-induced demyelination. We found that mice deficient in IL-17A, IL-17 receptor C (IL-17RC), and adaptor protein Act1 (of IL-17R) all had reduced demyelination accompanied by lessened microglial and polydendrocyte cellular reactivity compared with that in wild-type mice in response to cuprizone feeding, demonstrating the essential role of IL-17-induced Act1-mediated signaling in cuprizone-induced demyelination. Importantly, specific deletion of Act1 in astrocytes reduced the severity of tissue injury in this model, indicating the critical role of CNS resident cells in the pathogenesis of cuprizone-induced demyelination. In cuprizone-fed mice, IL-17 was produced by CNS CD3(+) T cells, suggesting a source of IL-17 in CNS upon cuprizone treatment.
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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.