Glutamate Receptor GluR3 Antibodies and Death of Cortical Cells
@article{He1998GlutamateRG, title={Glutamate Receptor GluR3 Antibodies and Death of Cortical Cells}, author={Xiao-ping He and Manisha N. Patel and Karl D. Whitney and Sridevi Janumpalli and Andrea J. Tenner and James O. McNamara}, journal={Neuron}, year={1998}, volume={20}, pages={153-163} }
118 Citations
Autoimmunity to the glutamate receptor in mice--a model for Rasmussen's encephalitis?
- BiologyJournal of autoimmunity
- 1999
Results suggest that autoimmunity to the GluR3B epitope may account for the neuronal death and brain pathology seen in neurodegenerative diseases like RE, but may not be sufficient to underly epilepsy, at least not in mice.
GluR3 Autoantibodies Destroy Neural Cells in a Complement-Dependent Manner Modulated by Complement Regulatory Proteins
- Biology, MedicineThe Journal of Neuroscience
- 2000
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.
Autoantibodies to the glutamate receptor kill neurons via activation of the receptor ion channel.
- BiologyJournal of autoimmunity
- 1999
Results show that antibodies to a specific peptide of the GluR can kill neurons by an excitotoxic mechanism, thus mimicking the effects of excess of glutamate, the first example that antibodies can lead to neuronal death in a non-classical complement-independent manner.
Autoantibodies to glutamate receptors can damage the brain in epilepsy, systemic lupus erythematosus and encephalitis
- Biology, MedicineExpert review of neurotherapeutics
- 2008
Epilepsy, autoimmune epilepsy, SLE and neuropsychiatric SLE in general is discussed; the up-to-date in vivo and in vitro evidence concerning the presence of glutamate receptor autoantibodies in human diseases is summarized; the activity and pathogenicity of different glutamate receptorAutoantibodied are discussed; and the conclusions, recommendations and suggested future directions are summarized.
Immunoglobulin G and complement immunoreactivity in the cerebral cortex of patients with Rasmussen’s encephalitis
- Medicine, BiologyNeurology
- 1999
Evidence that complement (C′)-dependent processes may be involved in Rasmussen’s encephalitis (RE) is provided, suggesting focal IgG-dependent classical C′ cascade pathway activation with attendant tissue damage in this subset of RE patients.
Absence of antibodies to glutamate receptor type 3 (GluR3) in Rasmussen encephalitis
- Medicine, BiologyNeurology
- 2004
GluR3 antibodies were only infrequently found in Rasmussen encephalitis or intractable epilepsy.
Dual-Targeted Autoimmune Sword in Fatal Epilepsy: Patient's glutamate receptor AMPA GluR3B peptide autoimmune antibodies bind, induce Reactive Oxygen Species (ROS) in, and kill both human neural cells and T cells.
- Biology, MedicineJournal of autoimmunity
- 2020
Immunization with the glutamate receptor-derived peptide GluR3B induces neuronal death and reactive gliosis, but confers partial protection from pentylenetetrazole-induced seizures
- BiologyExperimental Neurology
- 2005
Autoimmune Epilepsy: Some Epilepsy Patients Harbor Autoantibodies to Glutamate Receptors and dsDNA on both Sides of the Blood-brain Barrier, which may Kill Neurons and Decrease in Brain Fluids after Hemispherotomy
- Medicine, BiologyClinical & developmental immunology
- 2004
Some epilepsy patients harbor Ab's to GluR3 and dsDNA on both sides of the blood-brain barrier, and additional autoimmune Ab's only in serum, and since all these Ab's may be detrimental to the nervous system and/or peripheral organs, test for their presence in epilepsy, and silencing their activity in Ab-positive patients.
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