ArticlePloS one2012
Neuroinflammation by cytotoxic T-lymphocytes impairs retrograde axonal transport in an oligodendrocyte mutant mouse.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Inflammation's impact on the interaction between oligodendrocytes and axons.Discovery immunology · 2025Review
- Clinically approved immunomodulators ameliorate behavioral changes in a mouse model of hereditary spastic paraplegia type 11.Frontiers in neuroscience · 2024Article
- Microglia-mediated demyelination protects against CD8Nature communications · 2023Article
- Cytotoxic CNS-associated T cells drive axon degeneration by targeting perturbed oligodendrocytes iniScience · 2023Article
- Molecular Biology of Atherosclerotic Ischemic Strokes.International journal of molecular sciences · 2020Review
- Neuroinflammatory Mechanisms in Ischemic Stroke: Focus on Cardioembolic Stroke, Background, and Therapeutic Approaches.International journal of molecular sciences · 2020Review
- Corticohippocampal Dysfunction In The OBiden Mouse Model Of Primary Oligodendrogliopathy.Scientific reports · 2018Article
- Oxidative stress and mitochondrial dynamics malfunction are linked in Pelizaeus-Merzbacher disease.Brain pathology (Zurich, Switzerland) · 2018Article
- Teriflunomide attenuates neuroinflammation-related neural damage in mice carrying human PLP1 mutations.Journal of neuroinflammation · 2018Article
- Curcumin therapy in a Plp1 transgenic mouse model of Pelizaeus-Merzbacher disease.Annals of clinical and translational neurology · 2015Article
- Progesterone antagonist therapy in a Pelizaeus-Merzbacher mouse model.American journal of human genetics · 2014Article
- Clinically relevant intronic splicing enhancer mutation in myelin proteolipid protein leads to progressive microglia and astrocyte activation in white and gray matter regions of the brain.Journal of neuroinflammation · 2013Article
- Potential For Cell-mediated Immune Responses In Mouse Models Of Pelizaeus-Merzbacher Disease.Brain sciences · 2013Article
- Focal axonal swellings and associated ultrastructural changes attenuate conduction velocity in central nervous system axons: a computer modeling study.Physiological reports · 2013Article
- Histopathological lesions induced by stroke in the encephalon.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologieArticle
- Metabolic Alterations in Acute Cerebral Ischemia.Current health sciences journalArticle
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mice overexpressing proteolipid protein (PLP) develop a leukodystrophy-like disease involving cytotoxic, CD8+ T-lymphocytes. Here we show that these cytotoxic T-lymphocytes perturb retrograde axonal transport. Using fluorogold stereotactically injected into the colliculus superior, we found that PLP overexpression in oligodendrocytes led to significantly reduced retrograde axonal transport in retina ganglion cell axons. We also observed an accumulation of mitochondria in the juxtaparanodal axonal swellings, indicative for a disturbed axonal transport. PLP overexpression in the absence of T-lymphocytes rescued retrograde axonal transport defects and abolished axonal swellings. Bone marrow transfer from wildtype mice, but not from perforin- or granzyme B-deficient mutants, into lymphocyte-deficient PLP mutant mice led again to impaired axonal transport and the formation of axonal swellings, which are predominantly located at the juxtaparanodal region. This demonstrates that the adaptive immune system, including cytotoxic T-lymphocytes which release perforin and granzyme B, are necessary to perturb axonal integrity in the PLP-transgenic disease model. Based on our observations, so far not attended molecular and cellular players belonging to the immune system should be considered to understand pathogenesis in inherited myelin disorders with progressive axonal damage.
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