ArticleScientific reports2025
MHC class I and II expression and induction in oligodendrocytes varies with age.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed.
- Revisiting oligodendrocytes in amyotrophic lateral sclerosis using human multicellular stem cell models.Trends in cell biology · 2026Review
- Glial Cysteine Cathepsins: From Homeostasis to Neurodegeneration.Cellular and molecular neurobiology · 2026Review
- Oligodendroglia as Active Immunomodulators in Demyelinating Diseases.Neuroscience bulletin · 2026Review
- Stage-specific CHI3L1/YKL-40 signaling controls generation of oligodendrocyte precursor cells through IL13Rα2-mediated ferroptosis.bioRxiv : the preprint server for biology · 2026Article
- Enhanced myelination potential of human mature oligodendrocytes by TNF and IFNG combination.Journal of neuroinflammation · 2026Article
- Oligodendrocyte dysfunction in neurodegenerative diseases: pathological features, underlying mechanisms and therapeutic targeting.Frontiers in aging neuroscience · 2026Review
- Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Oligodendroglia expressing major histocompatibility complex (MHC) molecules have become of central interest in multiple sclerosis (MS) research, but their role in aging is still being elucidated. Using MHC class I and II reporter mice, we compared oligodendroglial MHC expression in neonatal, young adult (8-16 weeks), and aging (52 weeks) mice at baseline and after stereotactic delivery of AAV-GFAP-IFNγ. We found that MHC class I-expressing oligodendroglia were present in both the naïve brain and spinal cord, while MHC class II-expressing oligodendroglia were seen only in the spinal cord of aging mice at baseline. After AAV injection, MHC expression in oligodendroglia increased, recapitulating pathology seen in MS mouse models and in MS post-mortem tissue. After IFNγ-AAV injection, the abundance of MHC class I-expressing oligodendroglia did not vary with age, whereas MHC class II-expressing oligodendroglia were more abundant in aging mice than neonatal and young adult mice. Our results suggest that MHC class II-expressing oligodendroglia are more prevalent with aging, which may contribute to the mechanisms underlying progressive MS and other age-related neurodegenerative diseases with central nervous system 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 Socratic graph.