ArticleJournal of neuropathology and experimental neurology2009
Demyelinated axons and motor function are protected by genetic deletion of perforin in a mouse model of multiple sclerosis.
Article in Journal of neuropathology and experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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
33 citing papers in PubMed, 44 citations in OpenAlex.
- Pentose phosphate pathway inhibition metabolically reprograms CD8+ T cells and disrupts CNS autoimmunity.JCI insight · 2025Article
- CD8+ T cells recognizing a neuron-restricted antigen injure axons in a model of multiple sclerosis.The Journal of clinical investigation · 2023Article
- Marginal Zinc Deficiency during Gestation and Lactation in Rats Affects Oligodendrogenesis, Motor Performance, and Behavior in the Offspring.The Journal of nutrition · 2023Article
- Mice lacking perforin have improved regeneration of the injured femoral nerve.Neural regeneration research · 2022Article
- The CD8 T Cell-Epstein-Barr Virus-B Cell Trialogue: A Central Issue in Multiple Sclerosis Pathogenesis.Frontiers in immunology · 2021Review
- Encephalitogenic and Regulatory CD8 T Cells in Multiple Sclerosis and Its Animal Models.Journal of immunology (Baltimore, Md. : 1950) · 2021Review
- Targeting of Perforin Inhibitor into the Brain Parenchyma Via a Prodrug Approach Can Decrease Oxidative Stress and Neuroinflammation and Improve Cell Survival.Molecular neurobiology · 2020Article
- Effect of Fasudil on remyelination following cuprizone-induced demyelination.CNS neuroscience & therapeutics · 2020Article
- Comparison of Reported Spinal Cord Lesions in Progressive Multiple Sclerosis with Theiler's Murine Encephalomyelitis Virus Induced Demyelinating Disease.International journal of molecular sciences · 2019Article
- Calcium Influx through Plasma-Membrane Nanoruptures Drives Axon Degeneration in a Model of Multiple Sclerosis.Neuron · 2019Article
- The early proximal αβ TCR signalosome specifies thymic selection outcome through a quantitative protein interaction network.Science immunology · 2019Article
- Facets of Theiler's Murine Encephalomyelitis Virus-Induced Diseases: An Update.International journal of molecular sciences · 2019Review
- Retrograde interferon-gamma signaling induces major histocompatibility class I expression in human-induced pluripotent stem cell-derived neurons.Annals of clinical and translational neurology · 2018Article
- T-bet, but not Gata3, overexpression is detrimental in a neurotropic viral infection.Scientific reports · 2017Article
- Superior isolation of antigen-specific brain infiltrating T cells using manual homogenization technique.Journal of immunological methods · 2016Article
- Human class I major histocompatibility complex alleles determine central nervous system injury versus repair.Journal of neuroinflammation · 2016Article
- Levetiracetam Prevents Perforin Mediated Neuronal Injury Induced by Acute Cerebral Ischemia Reperfusion.Molecular neurobiology · 2016Article
- The Effect of Melatonin on Behavioral, Molecular, and Histopathological Changes in Cuprizone Model of Demyelination.Molecular neurobiology · 2016Article
- Organ-specific protective role of NKT cells in virus-induced inflammatory demyelination and myocarditis depends on mouse strain.Journal of neuroimmunology · 2015Article
- Th17-biased RORγt transgenic mice become susceptible to a viral model for multiple sclerosis.Brain, behavior, and immunity · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Axon injury is a major determinant of the loss of neurological function in patients with multiple sclerosis. It is unclear, however, whether damage to axons is an obligatory consequence of demyelination or whether it is an independent process that occurs in the permissive environment of demyelinated lesions. Previous investigations into the role of CD8 T cells and perforin in the Theiler murine encephalomyelitis virus model of multiple sclerosis have used mouse strains resistant to Theiler murine encephalomyelitis virus infection. To test the role of CD8 T cells in axon injury, we established a perforin-deficient mouse model on the H-2 major histocompatibility complex background thereby removing confounding factors related to viral biology in this Theiler murine encephalomyelitis virus-susceptible strain. This permitted direct comparison of clinical and pathological parameters between perforin-competent and perforin-deficient mice. The extent of demyelination was indistinguishable between perforin-competent and perforin-deficient H-2 mice, but chronically infected perforin-deficient mice exhibited preservation of motor function and spinal axons despite the presence of spinal cord demyelination. Thus, demyelination is necessary but insufficient for axon injury in this model; the absence of perforin protects axons without impacting demyelination. These results suggest that perforin is a key mediator of axon injury and lend additional support to the hypothesis that CD8 T cells are primarily responsible for axon damage in multiple sclerosis.
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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.