ArticleJournal of neurochemistry2011
Synergistic activity of interleukin-17 and tumor necrosis factor-α enhances oxidative stress-mediated oligodendrocyte apoptosis.
Article in Journal of neurochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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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.
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Who cites it
63 citing papers in PubMed, 106 citations in OpenAlex.
- Influence of a High-Impact Multidimensional Rehabilitation Program on the Gut Microbiota of Patients with Multiple Sclerosis.International journal of molecular sciences · 2021Trial
- M2-associated microglial states in oligodendrocyte regulation and white matter repair in vascular dementia.Journal of translational medicine · 2026Review
- Oligodendroglia as Active Immunomodulators in Demyelinating Diseases.Neuroscience bulletin · 2026Review
- Rethinking MS Therapeutics: From Disease Pathogenesis Mechanisms to AI-Driven Drug Discovery.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Review
- Amikacin toxicity revisited: pentoxifylline offers protection in high-risk treatment scenarios.AMB Express · 2025Article
- Moderate NADH supplementation prevents early colon carcinogenesis by modulating inflammation and oxidative stress in a mouse model.Journal of molecular histology · 2025Article
- Th17 cell pathogenicity in autoimmune disease.Experimental & molecular medicine · 2025Review
- The Quinazoline Derivative, QNZ, Alleviates Experimental Autoimmune Encephalomyelitis by Suppressing Th1 and Th17 Cells.CNS neuroscience & therapeutics · 2025Article
- Regulatory effect of inflammatory mediators in spinal cord injury.Frontiers in immunology · 2025Review
- Network Pharmacology Approach to Unveiling the Mechanism of Wolfberry Mulberry Raspberry Decoction in the Treatment of Sepsis-Induced Myocardial Dysfunction.Drug design, development and therapy · 2025Article
- Chronic Inflammation Offers Hints About Viable Therapeutic Targets for Preeclampsia and Potentially Related Offspring Sequelae.International journal of molecular sciences · 2024Review
- The Emerging Role of Phosphodiesterase 5 Inhibition in Neurological Disorders: The State of the Art.Cells · 2024Review
- Cellular and molecular mechanisms of the blood-brain barrier dysfunction in neurodegenerative diseases.Fluids and barriers of the CNS · 2024Review
- Parkinson's disease and schizophrenia interactomes contain temporally distinct gene clusters underlying comorbid mechanisms and unique disease processes.Schizophrenia (Heidelberg, Germany) · 2024Article
- Article
- T cells in health and disease.Signal transduction and targeted therapy · 2023Review
- Inflammatory Cytokines Associated with Multiple Sclerosis Directly Induce Alterations of Neuronal Cytoarchitecture in Human Neurons.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- An emerging role of inflammasomes in spinal cord injury and spinal cord tumor.Frontiers in immunology · 2023Review
- Unconventional T cells in brain homeostasis, injury and neurodegeneration.Frontiers in immunology · 2023Review
- Advances in the study of IL-17 in neurological diseases and mental disorders.Frontiers in neurology · 2023Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Th1 cytokine-induced loss of oligodendrocytes (OLs) is associated with axonal loss in CNS demyelinating diseases such as multiple sclerosis (MS)that contributes to neurological disabilities in affected individuals. Recent studies indicated that, in addition to Th1-phenotype cytokines including tumor necrosis factor (TNF)-α, Th17 phenotype cytokine, interleukin (IL)-17 also involved in the development of MS. In this study, we investigated the direct effect of IL-17 on the survival of OLs in the presence of TNF-α and individually in vitro settings. Our findings suggest that IL-17 alone, however, was not able to affect the survival of OLs, but it exacerbates the TNF-α-induced OL apoptosis as compared with individual TNF-α treatment. This effect of cytokines was ascribed to an inhibition of cell-survival mechanisms, co-localization of Bid/Bax proteins in the mitochondrial membrane and caspase 8 activation mediated release of apoptosis inducing factor from mitochondria in treated OLs. In addition, cytokine treatment disturbed the mitochondrial membrane potential in OLs with corresponding increase in the generation of reactive oxygen species, which were attenuated by N-acetyl cysteine treatment. In addition, combining of these cytokines induced cell-cycle arrest at G1/S phases in OL-like cells and inhibited the maturation of OL progenitor cells that was attenuated by peroxisome proliferator-activated receptor-γ/-β agonists. Collectively, these data provide initial evidence that IL-17 exacerbates TNF-α-induced OL loss and inhibits the differentiation of OL progenitor cells suggesting that antioxidant- or peroxisome proliferator-activated receptor agonist-based therapies have potential to limit CNS demyelination in MS or other related demyelinating disorders.
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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.