ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Immune cells contribute to myelin degeneration and axonopathic changes in mice overexpressing proteolipid protein in oligodendrocytes.
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 57 papers.
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57 citing papers in PubMed, 112 citations in OpenAlex.
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- New views on the complex interplay between degeneration and autoimmunity in multiple sclerosis.Frontiers in cellular neuroscience · 2024Article
- Microglia-mediated demyelination protects against CD8Nature communications · 2023Article
- Cytotoxic CNS-associated T cells drive axon degeneration by targeting perturbed oligodendrocytes iniScience · 2023Article
- Applications of Induced Pluripotent Stem Cell-Derived Glia in Brain Disease Research and Treatment.Handbook of experimental pharmacology · 2023Review
- Autophagic degradation of CNS myelin maintains axon integrity.Cell stress · 2022Article
- Interferon-driven brain phenotype in a mouse model of RNaseT2 deficient leukoencephalopathy.Nature communications · 2021Article
- Immune modulation attenuates infantile neuronal ceroid lipofuscinosis in mice before and after disease onset.Brain communications · 2021Article
- Neuron-Oligodendrocyte Interactions in the Structure and Integrity of Axons.Frontiers in cell and developmental biology · 2021Review
- Human Glial Progenitor Cells Effectively Remyelinate the Demyelinated Adult Brain.Cell reports · 2020Article
- Neural stem cells restore myelin in a demyelinating model of Pelizaeus-Merzbacher disease.Brain : a journal of neurology · 2020Article
- Absence of Plekhg5 Results in Myelin Infoldings Corresponding to an Impaired Schwann Cell Autophagy, and a Reduced T-Cell Infiltration Into Peripheral Nerves.Frontiers in cellular neuroscience · 2020Article
- Molecular mechanism for the multiple sclerosis risk variant rs17594362.Human molecular genetics · 2019Article
- Gene suppressing therapy for Pelizaeus-Merzbacher disease using artificial microRNA.JCI insight · 2019Article
- An in vitro model for studying CNS white matter: functional properties and experimental approaches.F1000Research · 2019Article
- Distinct VIP and PACAP Functions in the Distal Nerve Stump During Peripheral Nerve Regeneration.Frontiers in neuroscience · 2019Article
- Teriflunomide attenuates neuroinflammation-related neural damage in mice carrying human PLP1 mutations.Journal of neuroinflammation · 2018Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of the major myelin protein of the CNS, proteolipid protein (PLP), leads to late-onset degeneration of myelin and pathological changes in axons. Based on the observation that in white matter tracts of these mutants both CD8+ T-lymphocytes and CD11b+ macrophage-like cells are numerically elevated, we tested the hypothesis that these cells are pathologically involved in the primarily genetically caused neuropathy. Using flow cytometry of mutant brains, CD8+ cells could be identified as activated effector cells, and confocal microscopy revealed a close association of the T-cells with MHC-I+ (major histocompatibility complex class I positive) oligodendrocytes. Crossbreeding the myelin mutants with mice deficient in the recombination activating gene-1 (RAG-1) lacking mature T- and B-lymphocytes led to a reduction of the number of CD11b+ cells and to a substantial alleviation of pathological changes. In accordance with these findings, magnetic resonance imaging revealed less ventricular enlargement in the double mutants, partially because of more preserved corpora callosa. To investigate the role of CD8+ versus CD4+ T-lymphocytes, we reconstituted the myelin-RAG-1 double mutants with bone marrow from either CD8-negative (CD4+) or CD4-negative (CD8+) mice. The severe ventricular enlargement was only found when the double mutants were reconstituted with bone marrow from CD8+ mice, suggesting that the CD8+ lymphocytes play a critical role in the immune-related component of myelin degeneration in the mutants. These findings provide strong evidence that a primary glial damage can cause secondary immune reactions of pathological significance as it has been suggested for some forms of multiple sclerosis and other leukodystrophies.
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