ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
GluR3 autoantibodies destroy neural cells in a complement-dependent manner modulated by complement regulatory proteins.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
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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
28 citing papers in PubMed, 98 citations in OpenAlex.
- Enigmatic intractable Epilepsy patients have antibodies that bind glutamate receptor peptides, kill neurons, damage the brain, and cause Generalized Tonic Clonic Seizures.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- AMPA receptors in the evolving synapse: structure, function, and disease implications.Frontiers in synaptic neuroscience · 2025Review
- Non-canonical Roles of Complement in the CNS: From Synaptic Organizer to Presynaptic Modulator of Glutamate Transmission.Current neuropharmacology · 2025Review
- The correlation of GluR3B antibody with T lymphocyte subsets and inflammatory factors and their role in the progression of epilepsy.Journal of translational medicine · 2024Article
- Anti-NMDA and Anti-AMPA Receptor Antibodies in Central Disorders: Preclinical Approaches to Assess Their Pathological Role and Translatability to Clinic.International journal of molecular sciences · 2023Review
- The role of astrocytes in neuropathic pain.Frontiers in molecular neuroscience · 2022Review
- Structure, Function, and Pharmacology of Glutamate Receptor Ion Channels.Pharmacological reviews · 2021Review
- Autoimmune Epilepsy - Novel Multidisciplinary Analysis, Discoveries and Insights.Frontiers in immunology · 2021Review
- Antibodies Against the NHFrontiers in immunology · 2021Article
- Complement-dependent bystander injury to neurons in AQP4-IgG seropositive neuromyelitis optica.Journal of neuroinflammation · 2018Article
- Humanized mouse model of Rasmussen's encephalitis supports the immune-mediated hypothesis.The Journal of clinical investigation · 2018Article
- Bystander mechanism for complement-initiated early oligodendrocyte injury in neuromyelitis optica.Acta neuropathologica · 2017Article
- Anti-Hu antibodies activate enteric and sensory neurons.Scientific reports · 2016Article
- Autoantibodies in Neuropsychiatric Disorders.Antibodies (Basel, Switzerland) · 2016Review
- In Rasmussen encephalitis, hemichannels associated with microglial activation are linked to cortical pyramidal neuron coupling: a possible mechanism for cellular hyperexcitability.CNS neuroscience & therapeutics · 2015Article
- Review
- Immune response against ocular tissues after immunization with optic nerve antigens in a model of autoimmune glaucoma.Molecular vision · 2013Article
- Brain-reactive antibodies and disease.Annual review of immunology · 2013Review
- Article
- Neuroprotective effects of reactive oxygen species mediated by BDNF-independent activation of TrkB.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
GluR3 autoantibodies have been implicated in the development of Rasmussen's encephalitis, a rare neurodegenerative disease of humans characterized by epilepsy and degeneration of a single cerebral hemisphere. GluR3 autoantibodies are found in some Rasmussen's encephalitis patients, and GluR3 antibodies raised in rabbits destroy cultured cortical cells in a complement-dependent manner. In this study, the cellular targets of anti-GluR3 antisera-mediated cytotoxicity were examined in mixed primary neuronal-glial cultures of rat cortex. Unexpectedly, astrocytes were the principal target of the cytotoxic effects as assessed by immunohistochemistry and lactate dehydrogenase activity; neurons were destroyed to a lesser extent. Astrocyte vulnerability was rescued by transfection with complement regulatory proteins, and neuronal resistance was defeated by impairing complement regulatory protein function. Astrocyte death may occur in Rasmussen's encephalitis, and destruction of this cell type may play a critical role in the progression of this disorder. The present findings suggest complement regulatory protein expression may in part determine the nature and severity of Rasmussen's encephalitis and other complement-dependent nervous system diseases and thus underscore the need for a systematic investigation of the expression of all known complement regulatory proteins in healthy and diseased nervous system tissues.
Indexed as
Identifiers
11007888PMC6772766W1930520388What OpenQuestion holds
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.