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Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Type 1 narcolepsy: a CD8(+) T cell-mediated disease?

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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  1. CD8+ T cells from patients with narcolepsy and healthy controls recognize hypocretin neuron-specific antigens

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. In vivo clonal expansion and phenotypes of hypocretin-specific CD4+ T cells in narcolepsy patients and controls

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Altered surface expression of P2Y11 receptor with narcolepsy-associated mutations

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  4. Type 1 narcolepsy is not present in 29 HPV-vaccinated individuals with subjective sleep complaints

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  5. DNMT1 regulates expression of MHC class i in post-mitotic neurons

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Vis graf over relationer

Type 1 narcolepsy is a sleep disorder characterized by excessive daytime sleepiness with unintentional sleep attacks and cataplexy. The disorder is caused by a loss of hypocretinergic neurons in the brain. The specific loss of these neurons in narcolepsy is thought to result from an autoimmune attack, and this is supported by evidence of both environmental and genetic factors pointing toward an involvement of the immune system. However, definitive proof of an autoimmune etiology is still missing. Several different immune-mediated disorders targeting neurons are known, and many of these are believed to be caused by autoreactive CD8(+) T cells. In this paper, we review the current knowledge on CD8(+) T cell-mediated neuronal damage on the basis of our understanding of other autoimmune disorders and experimental studies. We identify major histocompatibility complex class I presentation of autoantigens on neurons as a possible mechanism in the development of the disease, and propose T cell-mediated pathogenesis, with cytotoxic CD8(+) T cells targeting the hypocretinergic neurons, as a central element.

OriginalsprogEngelsk
TidsskriftNew York Academy of Sciences. Annals
Vol/bind1351
Sider (fra-til)80-8
Antal sider9
ISSN0077-8923
DOI
StatusUdgivet - sep. 2015

ID: 45908138