ArticleActa neuropathologica2019
Microglial nodules provide the environment for pathogenic T cells in human encephalitis.
Article in Acta neuropathologica, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Pooled it
- International consensus recommendations for the diagnosis and treatment of Rasmussen syndrome: A modified Delphi procedure.Epilepsia · 2026Article
- Immune landscape of the affected brain in Rasmussen encephalitis.Scientific reports · 2026Article
- Microglial reactivity and nodule formation are associated with Synaptodendritic damage in the brains of people with HIV-1.Brain pathology (Zurich, Switzerland) · 2026Article
- Dual Role of Microglial TREM2 in Neuronal Degeneration and Regeneration After Axotomy.bioRxiv : the preprint server for biology · 2026Article
- Single-Nucleus Transcriptomics Reveals Cell Type-Specific Remodeling and Epilepsy-Associated Microglia.bioRxiv : the preprint server for biology · 2026Article
- The dynamics of brain T cell populations during the course of rasmussen encephalitis: from expansion to exhaustion.Journal of neuroinflammation · 2025Article
- Microglia aggregates define distinct immune and neurodegenerative niches in Alzheimer's disease hippocampus.Acta neuropathologica · 2025Article
- Potential inflammatory mechanisms of the ketogenic diet against febrile infection-related epilepsy syndrome.Acta epileptologica · 2025Review
- Age-dependent Powassan virus lethality is linked to glial cell activation and divergent neuroinflammatory cytokine responses in a murine model.Journal of virology · 2024Article
- Microglia contribute to polyG-dependent neurodegeneration in neuronal intranuclear inclusion disease.Acta neuropathologica · 2024Article
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- The neurobiology of SARS-CoV-2 infection.Nature reviews. Neuroscience · 2024Review
- Brain Leukocytes as the Potential Therapeutic Target for Post-COVID-19 Brain Fog.Neurochemical research · 2023Article
- Article
- Translational imaging of TSPO reveals pronounced innate inflammation in human and murine CD8 T cell-mediated limbic encephalitis.Science advances · 2023Article
- Temporal lobe epilepsy with GAD antibodies: neurons killed by T cells not by complement membrane attack complex.Brain : a journal of neurology · 2023Article
- Fetal Brain Damage in Human Fetuses with Congenital Cytomegalovirus Infection: Histological Features and Viral Tropism.Cellular and molecular neurobiology · 2023Article
- Immune Mechanisms in Epileptogenesis: Update on Diagnosis and Treatment of Autoimmune Epilepsy Syndromes.Drugs · 2023Review
- Brain molecular mechanisms in Rasmussen encephalitis.Epilepsia · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Microglia nodule formation is a common feature in inflammatory brain diseases mediated by T lymphocytes such as viral and paraneoplastic encephalitis, multiple sclerosis, and Rasmussen encephalitis (RE). However, its role has not been fully understood yet. We hypothesized that, in RE, microglial nodules provide an environment for the initiation of the later dominating T-cell cytotoxicity. In RE stage 0, small primary microglia nodules could be identified in the absence of T cells. These primary nodules showed inflammasome activation and endosomal Toll-like receptor upregulation. In stage 1, T cells migrate into the parenchyma and intermingle with microglial cells, thereby forming secondary nodules in which neurons are destroyed. Whole-genome transcriptome analysis at this point showed upregulation of several inflammatory pathways including interferon signaling and major histocompatibility complex-I signaling. Inflammatory profiles, like the ones observed in RE, could be induced upon TLR3 stimulation in neonatal microglial cell cultures. Taken together, our results point towards activation of endosomal TLRs, resulting in increased interferon signaling, inflammasome activation, and chemokine upregulation as early steps in RE pathogenesis. This activity sets the scene for subsequent infiltration of T cells and destruction of neurons. Similar to RE, this microglial microenvironment might be a crucial step in other T-cell-mediated inflammatory brain diseases.
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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 OpenQuestion graph.