ArticleProceedings of the National Academy of Sciences of the United States of America2021
Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 60 citations in OpenAlex.
- Review
- The Neurovascular Niche: A Gathering Venue for Neuroinflammation and Remyelination in Multiple Sclerosis.Acta physiologica (Oxford, England) · 2026Review
- Injury-transduced oligodendrocytes modulate neuroinflammation and glial activation in diseased and non-diseased central nervous system.Nature communications · 2026Article
- Role of CD5 signalling for pro-inflammatory Th17 response in multiple sclerosis.Brain : a journal of neurology · 2026Article
- Neurotransmitters as regulators of autoimmunity: mechanisms and translational targeting.NPJ autoimmunity · 2026Review
- The role of miRNAs in the development of Super-Tregs as a potential therapy for neurodegenerative diseases.Frontiers in immunology · 2026Review
- T cell-mediated immunodysregulation in multiple sclerosis: from pathogenic subsets to therapeutic advances.Frontiers in immunology · 2026Review
- Targeting O-GlcNAcylation: Novel Therapeutic Strategies for Neurological Disease.Molecular neurobiology · 2025Review
- Nanoparticle-boosted myeloid-derived suppressor cell therapy for immune reprogramming in multiple sclerosis.Science advances · 2025Article
- A pain from the nose to the head: neurological commitment during long COVID.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Review
- The shifting landscape of the preterm brain.Neuron · 2025Review
- Brain and Immune System: Intercellular Communication During Homeostasis and Neuroimmunomodulation upon Dysfunction.International journal of molecular sciences · 2025Review
- The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.Neuroscience bulletin · 2025Review
- Interaction between Th17 and central nervous system in multiple sclerosis.Brain, behavior, & immunity - health · 2025Review
- Novel insights into the ROCK-JAK-STAT signaling pathway in upper respiratory tract infections and neurodegenerative diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
- The immunological role of oligodendrocytes: beyond myelin maintenance.Discovery immunology · 2025Review
- Oligodendrocyte and Myelin Pathophysiology in Multiple Sclerosis.Advances in neurobiology · 2025Review
- Macrophage-targeted PEGylated liposomes ameliorate experimental autoimmune encephalomyelitis.Frontiers in immunology · 2025Article
- TNFR2 signaling in oligodendrocyte precursor cells suppresses their immune-inflammatory function and detrimental microglia activation in CNS demyelinating disease.Brain, behavior, and immunity · 2025Article
- Efficacy of Transcranial Direct Current Stimulation (tDCS) on Neuropsychiatric Symptoms in Multiple Sclerosis (MS)-A Review and Insight into Possible Mechanisms of Action.Journal of clinical medicine · 2024Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
T helper (Th)17 cells are considered to contribute to inflammatory mechanisms in diseases such as multiple sclerosis (MS). However, the discussion persists regarding their true role in patients. Here, we visualized central nervous system (CNS) inflammatory processes in models of MS live in vivo and in MS brains and discovered that CNS-infiltrating Th17 cells form prolonged stable contact with oligodendrocytes. Strikingly, compared to Th2 cells, direct contact with Th17 worsened experimental demyelination, caused damage to human oligodendrocyte processes, and increased cell death. Importantly, we found that in comparison to Th2 cells, both human and murine Th17 cells express higher levels of the integrin CD29, which is linked to glutamate release pathways. Of note, contact of human Th17 cells with oligodendrocytes triggered release of glutamate, which induced cell stress and changes in biosynthesis of cholesterol and lipids, as revealed by single-cell RNA-sequencing analysis. Finally, exposure to glutamate decreased myelination, whereas blockade of CD29 preserved oligodendrocyte processes from Th17-mediated injury. Our data provide evidence for the direct and deleterious attack of Th17 cells on the myelin compartment and show the potential for therapeutic opportunities in MS.
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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.