Autoimmune epilepsy (original) (raw)
- Correspondence
- Published: 01 June 2002
Nature Immunology volume 3, page 500 (2002)Cite this article
- 1997 Accesses
- 68 Citations
- Metrics details
An estimated 0.5–1% of the world population is epileptic, some with completely unknown etiology and no effective treatment. Epilepsies have long been viewed as diseases of the central nervous system (CNS), but in recent years, evidence has mounted that some may actually be autoimmune-mediated. If so, the way we regard and treat these epilepsies may require a revolutionary change. A session—which was sponsored by The Avraham and Sonia Rochlin Foundation—dealing, for the first time, with the “autoimmune epilepsy” concept took place in February 2002 at the International Congress of Autoimmunity in Geneva, Switzerland. Some salient findings reported at this session are relayed here.
The first clue to the autoimmune nature of some epilepsies came from the presence of antibodies to a major excitatory neurotransmitter in the CNS. Antibodies to this particular glutamate receptor, one of the AMPA (α-3-hydroxy-5-methyl-4-isoxazolepropionic acid) subtypes (GluR3), have now been found in three severe human epilepsies: Rasmussen's encephalitis (RE), noninflammatory focal epilepsy and “catastrophic” epilepsy (C. Antozzi & R. Montezzega, Italy). Specific cleavage of GluR3 by granzyme B, a serine protease released by activated immune cells, generates the GluR3B autoantigenic peptide, but only when an internal NH2-linked glycosylation sequence within the GluR3 recognition-sequence is not glycosylated (S. Rogers' group, USA). Interestingly, CD3+CD8+ cytotoxic T cells that contain granzyme B can be found in close association with neurons in the brains of RE patients and could contribute to neuronal death (H. Lassman's group, Austria).
This is a preview of subscription content, access via your institution
Relevant articles
Open Access articles citing this article.
The three pillars in treating antibody-mediated encephalitis
- S. Macher
- , G. Bsteh
- … P. S. Rommer
Wiener klinische Wochenschrift Open Access 06 June 2023
Access options
Subscribe to this journal
Receive 12 print issues and online access
$259.00 per year
only $21.58 per issue
Buy this article
- Purchase on SpringerLink
- Instant access to the full article PDF.
USD 39.95
Prices may be subject to local taxes which are calculated during checkout
Additional access options:
Author information
Authors and Affiliations
- The Sackler Faculty of Medicine, Tel Aviv University and The Weizmann Institute of Science, Rehovot, Israel
Mia Levite
Rights and permissions
About this article
Cite this article
Levite, M. Autoimmune epilepsy.Nat Immunol 3, 500 (2002). https://doi.org/10.1038/ni0602-500
- Issue date: 01 June 2002
- DOI: https://doi.org/10.1038/ni0602-500
This article is cited by
The three pillars in treating antibody-mediated encephalitis
- S. Macher
- G. Bsteh
- P. S. Rommer
Wiener klinische Wochenschrift (2024)
Neuroinflammatory mediators in acquired epilepsy: an update
- Yu Chen
- Marwa M. Nagib
- Jianxiong Jiang
Inflammation Research (2023)
Akut-symptomatische Anfälle infolge von Autoimmunenzephalitiden und autoimmun-assoziierte Epilepsien: Konzeptionelle Definitionen
- Christian G. Bien
Zeitschrift für Epileptologie (2020)
- Christian G. Bien
GLUTAMATE RECEPTOR ANTIBODIES IN NEUROLOGICAL DISEASES: Anti-AMPA-GluR3 antibodies, Anti-NMDA-NR1 antibodies, Anti-NMDA-NR2A/B antibodies, Anti-mGluR1 antibodies or Anti-mGluR5 antibodies are present in subpopulations of patients with either: Epilepsy, Encephalitis, Cerebellar Ataxia, Systemic Lupus Erythematosus (SLE) and Neuropsychiatric SLE, Sjogren’s syndrome, Schizophrenia, Mania or Stroke. These autoimmune anti-glutamate receptor antibodies can bind neurons in few brain regions, activate glutamate receptors, decrease glutamate receptor’s expression, impair glutamate-induced signaling and function, activate Blood Brain Barrier endothelial cells, kill neurons, damage the brain, induce behavioral/psychiatric/cognitive abnormalities and Ataxia in animal models, and can be removed or silenced in some patients by immunotherapy
- Mia Levite
Journal of Neural Transmission (2014)
- Mia Levite
Autoantibodies and neurodegeneration in multiple sclerosis
- Tamara Vyshkina
- Bernadette Kalman
Laboratory Investigation (2008)