A second major histocompatibility complex susceptibility locus for multiple sclerosis

Objective Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect originating from the HLA‐DRB1 gene in the class II region. The possibility that other genes in the MHC independently influence sus...

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Published inAnnals of neurology Vol. 61; no. 3; pp. 228 - 236
Main Authors Yeo, Tai Wai, De Jager, Philip L., Gregory, Simon G., Barcellos, Lisa F., Walton, Amie, Goris, An, Fenoglio, Chiara, Ban, Maria, Taylor, Craig J., Goodman, Reyna S., Walsh, Emily, Wolfish, Cara S., Horton, Roger, Traherne, James, Beck, Stephan, Trowsdale, John, Caillier, Stacy J., Ivinson, Adrian J., Green, Todd, Pobywajlo, Susan, Lander, Eric S., Pericak-Vance, Margaret A., Haines, Jonathan L., Daly, Mark J., Oksenberg, Jorge R., Hauser, Stephen L., Compston, Alastair, Hafler, David A., Rioux, John D., Sawcer, Stephen
Format Journal Article
LanguageEnglish
Published Hoboken Wiley Subscription Services, Inc., A Wiley Company 01.03.2007
Willey-Liss
Subjects
Adult
Biological and medical sciences
Female
Genetic Predisposition to Disease
HLA-D Antigens - genetics
Humans
Immunomodulators
Major Histocompatibility Complex - genetics
Male
Medical sciences
Microsatellite Repeats
Middle Aged
Multiple Sclerosis - genetics
Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis
Neurology
Original
Pharmacology. Drug treatments
Polymorphism, Single Nucleotide
Multiple sclerosis
Nervous system diseases
Locus
Major histocompatibility system
Central nervous system disease
Inflammatory disease
Online AccessGet full text

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Abstract Objective Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect originating from the HLA‐DRB1 gene in the class II region. The possibility that other genes in the MHC independently influence susceptibility to multiple sclerosis has been suggested but remains unconfirmed. Methods Using a combination of microsatellite, single nucleotide polymorphism, and human leukocyte antigen (HLA) typing, we screened the MHC in trio families looking for evidence of residual association above and beyond that attributable to the established DRB1*1501 risk haplotype. We then refined this analysis by extending the genotyping of classical HLA loci into independent cases and control subjects. Results Screening confirmed the presence of residual association and suggested that this was maximal in the region of the HLA‐C gene. Extending analysis of the classical loci confirmed that this residual association is partly due to allelic heterogeneity at the HLA‐DRB1 locus, but also reflects an independent effect from the HLA‐C gene. Specifically, the HLA‐C*05 allele, or a variant in tight linkage disequilibrium with it, appears to exert a protective effect (p = 3.3 × 10−5). Interpretation Variation in the HLA‐C gene influences susceptibility to multiple sclerosis independently of any effect attributable to the nearby HLA‐DRB1 gene. Ann Neurol 2007
AbstractList Objective Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect originating from the HLA-DRB1 gene in the class II region. The possibility that other genes in the MHC independently influence susceptibility to multiple sclerosis has been suggested but remains unconfirmed. Methods Using a combination of microsatellite, single nucleotide polymorphism, and human leukocyte antigen (HLA) typing, we screened the MHC in trio families looking for evidence of residual association above and beyond that attributable to the established DRB1*1501 risk haplotype. We then refined this analysis by extending the genotyping of classical HLA loci into independent cases and control subjects. Results Screening confirmed the presence of residual association and suggested that this was maximal in the region of the HLA-C gene. Extending analysis of the classical loci confirmed that this residual association is partly due to allelic heterogeneity at the HLA-DRB1 locus, but also reflects an independent effect from the HLA-C gene. Specifically, the HLA-C*05 allele, or a variant in tight linkage disequilibrium with it, appears to exert a protective effect (p = 3.3 X 10-5). Interpretation Variation in the HLA-C gene influences susceptibility to multiple sclerosis independently of any effect attributable to the nearby HLA-DRB1 gene. Ann Neurol 2007.
Objective Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect originating from the HLA‐DRB1 gene in the class II region. The possibility that other genes in the MHC independently influence susceptibility to multiple sclerosis has been suggested but remains unconfirmed. Methods Using a combination of microsatellite, single nucleotide polymorphism, and human leukocyte antigen (HLA) typing, we screened the MHC in trio families looking for evidence of residual association above and beyond that attributable to the established DRB1*1501 risk haplotype. We then refined this analysis by extending the genotyping of classical HLA loci into independent cases and control subjects. Results Screening confirmed the presence of residual association and suggested that this was maximal in the region of the HLA‐C gene. Extending analysis of the classical loci confirmed that this residual association is partly due to allelic heterogeneity at the HLA‐DRB1 locus, but also reflects an independent effect from the HLA‐C gene. Specifically, the HLA‐C*05 allele, or a variant in tight linkage disequilibrium with it, appears to exert a protective effect (p = 3.3 × 10−5). Interpretation Variation in the HLA‐C gene influences susceptibility to multiple sclerosis independently of any effect attributable to the nearby HLA‐DRB1 gene. Ann Neurol 2007
Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect originating from the HLA-DRB1 gene in the class II region. The possibility that other genes in the MHC independently influence susceptibility to multiple sclerosis has been suggested but remains unconfirmed.OBJECTIVEVariation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect originating from the HLA-DRB1 gene in the class II region. The possibility that other genes in the MHC independently influence susceptibility to multiple sclerosis has been suggested but remains unconfirmed.Using a combination of microsatellite, single nucleotide polymorphism, and human leukocyte antigen (HLA) typing, we screened the MHC in trio families looking for evidence of residual association above and beyond that attributable to the established DRB1*1501 risk haplotype. We then refined this analysis by extending the genotyping of classical HLA loci into independent cases and control subjects.METHODSUsing a combination of microsatellite, single nucleotide polymorphism, and human leukocyte antigen (HLA) typing, we screened the MHC in trio families looking for evidence of residual association above and beyond that attributable to the established DRB1*1501 risk haplotype. We then refined this analysis by extending the genotyping of classical HLA loci into independent cases and control subjects.Screening confirmed the presence of residual association and suggested that this was maximal in the region of the HLA-C gene. Extending analysis of the classical loci confirmed that this residual association is partly due to allelic heterogeneity at the HLA-DRB1 locus, but also reflects an independent effect from the HLA-C gene. Specifically, the HLA-C*05 allele, or a variant in tight linkage disequilibrium with it, appears to exert a protective effect (p = 3.3 x 10(-5)).RESULTSScreening confirmed the presence of residual association and suggested that this was maximal in the region of the HLA-C gene. Extending analysis of the classical loci confirmed that this residual association is partly due to allelic heterogeneity at the HLA-DRB1 locus, but also reflects an independent effect from the HLA-C gene. Specifically, the HLA-C*05 allele, or a variant in tight linkage disequilibrium with it, appears to exert a protective effect (p = 3.3 x 10(-5)).Variation in the HLA-C gene influences susceptibility to multiple sclerosis independently of any effect attributable to the nearby HLA-DRB1 gene.INTERPRETATIONVariation in the HLA-C gene influences susceptibility to multiple sclerosis independently of any effect attributable to the nearby HLA-DRB1 gene.
Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect originating from the HLA-DRB1 gene in the class II region. The possibility that other genes in the MHC independently influence susceptibility to multiple sclerosis has been suggested but remains unconfirmed. Using a combination of microsatellite, single nucleotide polymorphism, and human leukocyte antigen (HLA) typing, we screened the MHC in trio families looking for evidence of residual association above and beyond that attributable to the established DRB1*1501 risk haplotype. We then refined this analysis by extending the genotyping of classical HLA loci into independent cases and control subjects. Screening confirmed the presence of residual association and suggested that this was maximal in the region of the HLA-C gene. Extending analysis of the classical loci confirmed that this residual association is partly due to allelic heterogeneity at the HLA-DRB1 locus, but also reflects an independent effect from the HLA-C gene. Specifically, the HLA-C*05 allele, or a variant in tight linkage disequilibrium with it, appears to exert a protective effect (p = 3.3 x 10(-5)). Variation in the HLA-C gene influences susceptibility to multiple sclerosis independently of any effect attributable to the nearby HLA-DRB1 gene.
Author Wolfish, Cara S.
Goodman, Reyna S.
Traherne, James
Horton, Roger
Beck, Stephan
Sawcer, Stephen
Trowsdale, John
Caillier, Stacy J.
Green, Todd
Rioux, John D.
Hafler, David A.
Gregory, Simon G.
Fenoglio, Chiara
Walton, Amie
Hauser, Stephen L.
Yeo, Tai Wai
Walsh, Emily
Ban, Maria
Barcellos, Lisa F.
Lander, Eric S.
Goris, An
Daly, Mark J.
Haines, Jonathan L.
Compston, Alastair
Taylor, Craig J.
Pobywajlo, Susan
Pericak-Vance, Margaret A.
Ivinson, Adrian J.
Oksenberg, Jorge R.
De Jager, Philip L.
AuthorAffiliation 7 Division of Epidemiology, School of Public Health, University of California at Berkeley Berkeley, CA
15 Institute for Human Genetics, School of Medicine, University of California San Francisco San Francisco, CA
6 Department of Neurology, School of Medicine, University of California San Francisco San Francisco
5 Duke University Medical Center, Center for Human Genetics Durham, NC
1 Department of Clinical Neurosciences, University of Cambridge, Addenbrooke's Hospital Cambridge, United Kingdom
10 Wellcome Trust Sanger Institute, Genome Campus Hinxton, United Kingdom
4 Program in Medical and Population Genetics, The Broad Institute at the Massachusetts Institute of Technology and Harvard University Cambridge, MA
9 Tissue Typing Laboratory, Addenbrooke's Hospital United Kingdom
13 The Center for Genome Research, Massachusetts General Hospital Boston, MA
16 Montréal Heart Institute and Université de Montréal Montréal, Québec, Canada
8 Department of Neurological Sciences, Dino Ferrari Center, Univers
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– name: 16 Montréal Heart Institute and Université de Montréal Montréal, Québec, Canada
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– name: 12 Harvard Center for Neurodegeneration and Repair Boston, MA
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– name: 3 Harvard Medical School Boston
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https://www.ncbi.nlm.nih.gov/pubmed/17252545$$D View this record in MEDLINE/PubMed
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Issue 3
Keywords Multiple sclerosis
Nervous system diseases
Locus
Major histocompatibility system
Central nervous system disease
Inflammatory disease
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
CC BY 4.0
Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.
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Notes European Neurological Society fellowship
Wellcome Trust - No. 048880; No. 057097
Cancer Research Institute fellowship
Wellcome Trust Prize Studentship
National Multiple Sclerosis Society Center Grant - No. AP 3758-A-16
Cambridge Commonwealth Trust and Cambridge Philosophical Society
Postdoctoral Fellowship of the Research Foundation-Flanders (FWO-Vlaanderen)
ark:/67375/WNG-P8B13M68-0
GlaxoSmithKline Clinical Fellowship
istex:FD341487A234405A5B7C443E02FFBED99AD702EC
National Institutes of Health - No. K08 NS46341; No. NS049477; No. NS026799; No. NS032830
Medical Research Council (United Kingdom) - No. G0000648
ArticleID:ANA21063
St. Edmund's College
William C. Fowler scholarship in Multiple Sclerosis
The Penates Foundation
T.W.Y. and P.L.D. contributed equally to this work.
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2004; 63
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1998; 87
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2003; 73
1989; 25
2001; 69
1972; 1
2004; 53
2005; 201
2004; 14
2003; 25
2002; 70
1996; 273
1998; 7
2003; 143
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References_xml – reference: Vartdal F, Sollid LM, Vandvik B, et al. Patients with multiple sclerosis carry DQB1 genes which encode shared polymorphic amino acid sequences. Hum Immunol 1989; 25: 103-110.
– reference: Dudbridge F. Pedigree disequilibrium tests for multilocus haplotypes. Genet Epidemiol 2003; 25: 115-121.
– reference: Tamiya G, Shiina T, Oka A, et al. New polymorphic microsatellite markers in the human MHC class I region. Tissue Antigens 1999; 54: 221-228.
– reference: Skol AD, Scott LJ, Abecasis GR, Boehnke M. Joint analysis is more efficient than replication-based analysis for two-stage genome-wide association studies. Nat Genet 2006; 38: 209-213.
– reference: Rogner UC, Avner P. Congenic mice: cutting tools for complex immune disorders. Nat Rev Immunol 2003; 3: 243-252.
– reference: Florez JC, Burtt N, de Bakker PI, et al. Haplotype structure and genotype-phenotype correlations of the sulfonylurea receptor and the islet ATP-sensitive potassium channel gene region. Diabetes 2004; 53: 1360-1368.
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Snippet Objective Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the...
Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the strongest effect...
Objective Variation in the major histocompatibility complex (MHC) on chromosome 6p21 is known to influence susceptibility to multiple sclerosis with the...
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StartPage 228
SubjectTerms Adult
Biological and medical sciences
Female
Genetic Predisposition to Disease
HLA-D Antigens - genetics
Humans
Immunomodulators
Major Histocompatibility Complex - genetics
Male
Medical sciences
Microsatellite Repeats
Middle Aged
Multiple Sclerosis - genetics
Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis
Neurology
Original
Pharmacology. Drug treatments
Polymorphism, Single Nucleotide
Title A second major histocompatibility complex susceptibility locus for multiple sclerosis
URI https://api.istex.fr/ark:/67375/WNG-P8B13M68-0/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fana.21063
https://www.ncbi.nlm.nih.gov/pubmed/17252545
https://www.proquest.com/docview/19736847
https://www.proquest.com/docview/70326297
https://pubmed.ncbi.nlm.nih.gov/PMC2737610
Volume 61
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