Narcolepsy with hypocretin/orexin deficiency, infections and autoimmunity of the brain
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Narcolepsy with hypocretin/orexin deficiency, infections and autoimmunity of the brain. / Kornum, Birgitte Rahbek; Faraco, Juliette; Mignot, Emmanuel.
In: Current Opinion in Neurobiology, Vol. 21, No. 6, 12.2011, p. 897-903.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Narcolepsy with hypocretin/orexin deficiency, infections and autoimmunity of the brain
AU - Kornum, Birgitte Rahbek
AU - Faraco, Juliette
AU - Mignot, Emmanuel
N1 - Copyright © 2011 Elsevier Ltd. All rights reserved.
PY - 2011/12
Y1 - 2011/12
N2 - The loss of hypothalamic hypocretin/orexin (hcrt) producing neurons causes narcolepsy with cataplexy. An autoimmune basis for the disease has long been suspected and recent results have greatly strengthened this hypothesis. Narcolepsy with hcrt deficiency is now known to be associated with a Human Leukocyte Antigen (HLA) and T-cell receptor (TCR) polymorphisms, suggesting that an autoimmune process targets a single peptide unique to hcrt-cells via specific HLA-peptide-TCR interactions. Recent data have shown a robust seasonality of disease onset in children and associations with Streptococcus Pyogenes, and influenza A H1N1-infection and H1N1-vaccination, pointing towards processes such as molecular mimicry or bystander activation as crucial for disease development. We speculate that upper airway infections may be common precipitants of a whole host of CNS autoimmune complications including narcolepsy.
AB - The loss of hypothalamic hypocretin/orexin (hcrt) producing neurons causes narcolepsy with cataplexy. An autoimmune basis for the disease has long been suspected and recent results have greatly strengthened this hypothesis. Narcolepsy with hcrt deficiency is now known to be associated with a Human Leukocyte Antigen (HLA) and T-cell receptor (TCR) polymorphisms, suggesting that an autoimmune process targets a single peptide unique to hcrt-cells via specific HLA-peptide-TCR interactions. Recent data have shown a robust seasonality of disease onset in children and associations with Streptococcus Pyogenes, and influenza A H1N1-infection and H1N1-vaccination, pointing towards processes such as molecular mimicry or bystander activation as crucial for disease development. We speculate that upper airway infections may be common precipitants of a whole host of CNS autoimmune complications including narcolepsy.
KW - Autoimmune Diseases/immunology
KW - Brain/immunology
KW - Humans
KW - Intracellular Signaling Peptides and Proteins/deficiency
KW - Narcolepsy/immunology
KW - Neuropeptides/deficiency
KW - Orexins
U2 - 10.1016/j.conb.2011.09.003
DO - 10.1016/j.conb.2011.09.003
M3 - Review
C2 - 21963829
VL - 21
SP - 897
EP - 903
JO - Current Opinion in Neurobiology
JF - Current Opinion in Neurobiology
SN - 0959-4388
IS - 6
ER -
ID: 196168832