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}
}
View on Elsevier
cell.com
118 Citations
Highly Influential Citations
5
Background Citations
37
Methods Citations
2
Results Citations
7

Figures from this paper

118 Citations

Citation Type

Citation Type

Autoimmunity to the glutamate receptor in mice--a model for Rasmussen's encephalitis?
TLDR
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
TLDR
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.
TLDR
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
TLDR
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
TLDR
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
TLDR
GluR3 antibodies were only infrequently found in Rasmussen encephalitis or intractable epilepsy.
Autoimmunity to Munc-18 in Rasmussen's Encephalitis
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.
Immunization with the glutamate receptor-derived peptide GluR3B induces neuronal death and reactive gliosis, but confers partial protection from pentylenetetrazole-induced seizures
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
TLDR
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.
...
...

References

SHOWING 1-10 OF 54 REFERENCES
Autoantibodies to glutamate receptor GluR3 in Rasmussen's encephalitis.
TLDR
Repeated plasma exchanges in one seriously ill child transiently reduced serum titers of GluR3 antibodies, decreased seizure frequency, and improved neurologic function, suggesting an autoimmune process may underlie Rasmussen's encephalitis.
Glutamate receptor antibodies activate a subset of receptors and reveal an agonist binding site
Immune system response in Alzheimer's disease.
TLDR
It is established that astrocytes, which are GFAP positive, do not express MHC antigens in Alzheimer's disease, and that reactive microglia and some leukocytes express class II antigen.
The segregation and expression of glutamate receptor subunits in cultured hippocampal neurons
Update on the syndrome of "chronic encephalitis" and epilepsy.
TLDR
A retrospective review of 512 consecutive surgical specimens from patients operated upon at the MNI for medically refractory focal seizures gave confirmatory evidence that when focal seizures were associated with slowly progressive neurologic deterioration, the probable cause was a chronic, encephalitis-like condition.
Plasmapheresis in Rasmussen's encephalitis
TLDR
Observations indicate that circulating factors, likely autoantibodies, are pathogenic in at least some patients with RE and suggest that RE is an autoimmune disease and may be a useful adjunctive therapy in RE.
Intraneuronal IgG in the central nervous system
The Membrane Attack Complex of Complement at the Endplate in Myasthenia Gravis a
TLDR
The frequency of complement-mediated damage at the MG endplate is evaluated by paired fluorescence localization in the same sections of the neoantigenic determinants of the C5b-9 complement membrane attack complex (MAC) and AChR and to compare the relative reactivities for ACh R and MAC at the same endplates.
Evidence for multiple AMPA receptor complexes in hippocampal CA1/CA2 neurons
TLDR
The results show that AMPA receptor complexes with different subunit compositions are present in CA1/CA2 pyramidal neurons and suggest an additional mechanism to regulate receptor expression in neurons.
Soluble human complement receptor type 1: in vivo inhibitor of complement suppressing post-ischemic myocardial inflammation and necrosis.
TLDR
The sCR1 had complement inhibitory and anti-inflammatory activities in a rat model of reperfusion injury of ischemic myocardium, reducing myocardial infarction size by 44 percent and is identified as a potential agent for the suppression of complement-dependent tissue injury in autoimmune and inflammatory diseases.
...
...