ArticleAnnals of neurology2007
Astrocytes are a specific immunological target in Rasmussen's encephalitis.
Article in Annals of neurology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 164 citations in OpenAlex.
- Single-Cell Dissection of the SPP1-CD44 Axis Reveals Microglia-Astrocyte Crosstalk Driving Neuroinflammation in Temporal Lobe Epilepsy.Molecular neurobiology · 2026Article
- Longitudinal PET and MRI Evaluation in Late Onset Rasmussen Encephalitis: A Series of Three Cases.European journal of neurology · 2025Article
- The Role of Neuroinflammation and Network Anomalies in Drug-Resistant Epilepsy.Neuroscience bulletin · 2025Review
- Subcortical plaques and inflammation reflect cortical and meningeal pathologies in progressive multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2025Article
- The immune system and metabolic products in epilepsy and glioma-associated epilepsy: emerging therapeutic directions.JCI insight · 2024Review
- The Role of the Vagus Nerve in the Microbiome and Digestive System in Relation to Epilepsy.Current medicinal chemistry · 2024Review
- Single-Cell Sequencing Combined with Transcriptome Sequencing Constructs a Predictive Model of Key Genes in Multiple Sclerosis and Explores Molecular Mechanisms Related to Cellular Communication.Journal of inflammation research · 2024Article
- Myeloid cell iron uptake pathways and paramagnetic rim formation in multiple sclerosis.Acta neuropathologica · 2023Article
- Rasmussen's Encephalitis: A Literary Review.Cureus · 2023Review
- Factors not considered in the study of drug-resistant epilepsy: Drug-resistant epilepsy: Assessment of neuroinflammation.Epilepsia open · 2022Review
- The role of astrocytes in epileptic disorders.Physiological reports · 2022Review
- The role of astrocytes in neuropathic pain.Frontiers in molecular neuroscience · 2022Review
- Impact of T cells on neurodegeneration in anti-GAD65 limbic encephalitis.Annals of clinical and translational neurology · 2021Article
- Fundamental mechanistic insights from rare but paradigmatic neuroimmunological diseases.Nature reviews. Neurology · 2021Review
- The CD8 T Cell-Epstein-Barr Virus-B Cell Trialogue: A Central Issue in Multiple Sclerosis Pathogenesis.Frontiers in immunology · 2021Review
- Brain astrocytes and microglia express functional MR1 molecules that present microbial antigens to mucosal-associated invariant T (MAIT) cells.Journal of neuroimmunology · 2020Article
- An immunotherapy effect analysis in Rasmussen encephalitis.BMC neurology · 2020Article
- Rasmussen's encephalitis: mechanisms update and potential therapy target.Therapeutic advances in chronic disease · 2020Review
- Interleukin 4 Affects Epilepsy by Regulating Glial Cells: Potential and Possible Mechanism.Frontiers in molecular neuroscience · 2020Review
- Autoimmune seizures and epilepsy.The Journal of clinical investigation · 2019Review
10 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe current histopathological criteria of Rasmussen's encephalitis (RE) include the presence of T-cell-dominated inflammation, microglial activation, neuronal loss, and astrocytic activation. An in vitro study, however, suggested glutamate receptor 3 (GluR3) antibody-mediated astrocytic loss. Therefore, we investigated astrocytic apoptosis and loss in situ.
methodsHistochemical, immunohistochemical, terminal deoxynucleotidyltransferase-mediated biotin-dUTP nick end labeling and in situ hybridization techniques were applied to paraffin sections of 20 RE cases, 6 healthy control subjects, and 6 paraneoplastic encephalomyelitis, 10 Ammon's horn sclerosis, and 5 focal cortical dysplasia cases.
resultsAstrocytic apoptosis and subsequent loss of these cells is a specific feature of RE. Such lesions are not found in the control groups. In RE, astrocytic apoptosis and loss was present both in cortical and in white matter areas. Astrocytes in these tissues showed major histocompatibility complex class I expression. Furthermore, granzyme-B(+) lymphocytes were found in close apposition to astrocytes bordering astrocyte-deficient lesions. Granzyme-B(+) granules in these lymphocytes were polarized and faced the astrocytic membranes. No evidence was found for an antibody-mediated destruction.
interpretationWe suggest a specific attack by cytotoxic T lymphocytes as a possible mechanism responsible for astrocytic degeneration in RE. The loss of astrocytes might play a role in neuronal dysfunction, seizure induction, and enhancement of neuronal cell death.
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