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Title: ImmunoChip Study Implicates Antigen Presentation to T Cells in Narcolepsy
Author(s): Faraco, J.; Lin, L.; Kornum, B.R.; Kenny, E.E.; Trynka, G.; Einen, M.; Rico, T.J.; Lichtner, P.; Dauvilliers, Y.; Arnulf, I.; Lecendreux, M.; Javidi, S.; Geisler, P.; Mayer, G.; Pizza, F.; Poli, F.; Plazzi, G.; Overeem, S. ; Lammers, G.J.; Kemlink, D.; Sonka, K.; Nevsimalova, S.; Rouleau, G.; Desautels, A.; Montplaisir, J.; Frauscher, B.; Ehrmann, L.; Hogl, B.; Jennum, P.; Bourgin, P.; Peraita-Adrados, R.; Iranzo, A.; Bassetti, C.; Chen, W.M.; Concannon, P.; Thompson, S.D.; Damotte, V.; Fontaine, B.; Breban, M.; Gieger, C.; Klopp, N.; Deloukas, P.; Wijmenga, C.; Hallmayer, J.; Onengut-Gumuscu, S.; Rich, S.S.; Winkelmann, J.; Mignot, E.
Publication year: 2013
Source: Plos Genetics, vol. 9, iss. 2, (2013), pp. e1003270
ISSN: 1553-7404
DOI: http://dx.doi.org/10.1371/journal.pgen.1003270
Publication type: Article / Letter to editor

Please use this identifier to cite or link to this item : https://hdl.handle.net/2066/118596   https://hdl.handle.net/2066/118596

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Subject: DCN MP - Plasticity and memory
Organization: Neurology
Journal title:
Plos Genetics
Volume: vol. 9
Issue: iss. 2
Page start: p. e1003270
Abstract:
Recent advances in the identification of susceptibility genes and environmental exposures provide broad support for a post-infectious autoimmune basis for narcolepsy/hypocretin (orexin) deficiency. We genotyped loci associated with other autoimmune and inflammatory diseases in 1,886 individuals with hypocretin-deficient narcolepsy and 10,421 controls, all of European ancestry, using a custom genotyping array (ImmunoChip). Three loci located outside the Human Leukocyte Antigen (HLA) region on chromosome 6 were significantly associated with disease risk. In addition to a strong signal in the T cell receptor alpha (TRA@), variants in two additional narcolepsy loci, Cathepsin H () and Tumor necrosis factor (ligand) superfamily member 4 (, also called ), attained genome-wide significance. These findings underline the importance of antigen presentation by HLA Class II to T cells in the pathophysiology of this autoimmune disease.

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