期刊
PLOS GENETICS
卷 9, 期 2, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pgen.1003270
关键词
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资金
- Wake Up Narcolepsy
- EU-NN
- UCB Pharma
- PHRC [07-0138]
- Assistance Publique-Hopitaux de Paris
- French Ministry of Research and Higher Education
- Project Agence Nationale de la Recherche-07-MRAR (France)
- Czech Republic [MSM0021620849]
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
- National Institute of Allergy and Infectious Diseases (NIAID)
- National Human Genome Research Institute (NHGRI)
- National Institute of Child Health and Human Development (NICHD)
- Juvenile Diabetes Research Foundation International (JDRF)
- NIH [U01 DK062418, RC1AR058587, U01 AI067150]
- UK Medical Research Council [G0000934]
- Wellcome Trust [068545/Z/02]
- Helmholtz Zentrum Munchen-German Research Center for Environmental Health
- German Federal Ministry of Education and Research (BMBF)
- State of Bavaria
- Furthermore
- KORA within the Munich Center of Health Sciences (MC Health)
- Ludwig-Maximilians-Universitat, as part of LMUinnovativ
- INSERM
- ARSEP
- CRB-REFGENSEP
- Cincinnati Children's Hospital Research Foundation
- MRC [G0000934] Funding Source: UKRI
- Medical Research Council [G0000934] Funding Source: researchfish
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 (CTSH) and Tumor necrosis factor (ligand) superfamily member 4 (TNFSF4, also called OX40L), 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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