Fine-mapping the genetic association of the major histocompatibility complex in multiple sclerosis: HLA and non-HLA effects
The major histocompatibility complex (MHC) region is strongly associated with multiple sclerosis (MS) susceptibility. HLA-DRB1*15:01 has the strongest effect, and several other alleles have been reported at different levels of validation. Using SNP data from genome-wide studies, we imputed and teste...
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| Veröffentlicht in: | PLoS genetics 2013-11, Vol.9 (11), p.e1003926 |
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| creator | Patsopoulos, Nikolaos A Barcellos, Lisa F Hintzen, Rogier Q Schaefer, Catherine van Duijn, Cornelia M Noble, Janelle A Raj, Towfique Gourraud, Pierre-Antoine Stranger, Barbara E Oksenberg, Jorge Olsson, Tomas Taylor, Bruce V Sawcer, Stephen Hafler, David A Carrington, Mary De Jager, Philip L de Bakker, Paul I W |
| description | The major histocompatibility complex (MHC) region is strongly associated with multiple sclerosis (MS) susceptibility. HLA-DRB1*15:01 has the strongest effect, and several other alleles have been reported at different levels of validation. Using SNP data from genome-wide studies, we imputed and tested classical alleles and amino acid polymorphisms in 8 classical human leukocyte antigen (HLA) genes in 5,091 cases and 9,595 controls. We identified 11 statistically independent effects overall: 6 HLA-DRB1 and one DPB1 alleles in class II, one HLA-A and two B alleles in class I, and one signal in a region spanning from MICB to LST1. This genomic segment does not contain any HLA class I or II genes and provides robust evidence for the involvement of a non-HLA risk allele within the MHC. Interestingly, this region contains the TNF gene, the cognate ligand of the well-validated TNFRSF1A MS susceptibility gene. The classical HLA effects can be explained to some extent by polymorphic amino acid positions in the peptide-binding grooves. This study dissects the independent effects in the MHC, a critical region for MS susceptibility that harbors multiple risk alleles. |
| doi_str_mv | 10.1371/journal.pgen.1003926 |
| format | Article |
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HLA-DRB1*15:01 has the strongest effect, and several other alleles have been reported at different levels of validation. Using SNP data from genome-wide studies, we imputed and tested classical alleles and amino acid polymorphisms in 8 classical human leukocyte antigen (HLA) genes in 5,091 cases and 9,595 controls. We identified 11 statistically independent effects overall: 6 HLA-DRB1 and one DPB1 alleles in class II, one HLA-A and two B alleles in class I, and one signal in a region spanning from MICB to LST1. This genomic segment does not contain any HLA class I or II genes and provides robust evidence for the involvement of a non-HLA risk allele within the MHC. Interestingly, this region contains the TNF gene, the cognate ligand of the well-validated TNFRSF1A MS susceptibility gene. The classical HLA effects can be explained to some extent by polymorphic amino acid positions in the peptide-binding grooves. This study dissects the independent effects in the MHC, a critical region for MS susceptibility that harbors multiple risk alleles.</description><identifier>ISSN: 1553-7404</identifier><identifier>ISSN: 1553-7390</identifier><identifier>EISSN: 1553-7404</identifier><identifier>DOI: 10.1371/journal.pgen.1003926</identifier><identifier>PMID: 24278027</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alleles ; Amino acids ; Biomedical research ; Chromosome Mapping ; Councils ; Genetic aspects ; Genetic Predisposition to Disease ; Genetic screening ; Genome-Wide Association Study ; Genomes ; Haplotypes ; Health aspects ; Histocompatibility antigens ; Histocompatibility Antigens Class I - genetics ; HLA histocompatibility antigens ; HLA-DP beta-Chains - genetics ; HLA-DRB1 Chains - genetics ; Humans ; Intracellular Signaling Peptides and Proteins ; Linkage Disequilibrium ; Major histocompatibility complex ; Major Histocompatibility Complex - genetics ; Medical research ; Membrane Proteins - genetics ; Methods ; Multiple sclerosis ; Multiple Sclerosis - genetics ; Multiple Sclerosis - pathology ; Physiological aspects ; Polymorphism, Single Nucleotide ; Receptors, Tumor Necrosis Factor, Type I - genetics ; Studies</subject><ispartof>PLoS genetics, 2013-11, Vol.9 (11), p.e1003926</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013</rights><rights>2013 Public Library of Science. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited: Citation: Patsopoulos NA, Barcellos LF, Hintzen RQ, Schaefer C, van Duijn CM, et al. (2013) Fine-Mapping the Genetic Association of the Major Histocompatibility Complex in Multiple Sclerosis: HLA and Non-HLA Effects. PLoS Genet 9(11): e1003926. doi:10.1371/journal.pgen.1003926</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c802t-613331a94ca042bf613ccdb51dd570f645748d501f198e700abef7241d3e16003</citedby><cites>FETCH-LOGICAL-c802t-613331a94ca042bf613ccdb51dd570f645748d501f198e700abef7241d3e16003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836799/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3836799/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,551,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24278027$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:128223749$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><contributor>Gibson, Greg</contributor><creatorcontrib>Patsopoulos, Nikolaos A</creatorcontrib><creatorcontrib>Barcellos, Lisa F</creatorcontrib><creatorcontrib>Hintzen, Rogier Q</creatorcontrib><creatorcontrib>Schaefer, Catherine</creatorcontrib><creatorcontrib>van Duijn, Cornelia M</creatorcontrib><creatorcontrib>Noble, Janelle A</creatorcontrib><creatorcontrib>Raj, Towfique</creatorcontrib><creatorcontrib>Gourraud, Pierre-Antoine</creatorcontrib><creatorcontrib>Stranger, Barbara E</creatorcontrib><creatorcontrib>Oksenberg, Jorge</creatorcontrib><creatorcontrib>Olsson, Tomas</creatorcontrib><creatorcontrib>Taylor, Bruce V</creatorcontrib><creatorcontrib>Sawcer, Stephen</creatorcontrib><creatorcontrib>Hafler, David A</creatorcontrib><creatorcontrib>Carrington, Mary</creatorcontrib><creatorcontrib>De Jager, Philip L</creatorcontrib><creatorcontrib>de Bakker, Paul I W</creatorcontrib><creatorcontrib>IMSGC</creatorcontrib><creatorcontrib>ANZgene</creatorcontrib><title>Fine-mapping the genetic association of the major histocompatibility complex in multiple sclerosis: HLA and non-HLA effects</title><title>PLoS genetics</title><addtitle>PLoS Genet</addtitle><description>The major histocompatibility complex (MHC) region is strongly associated with multiple sclerosis (MS) susceptibility. HLA-DRB1*15:01 has the strongest effect, and several other alleles have been reported at different levels of validation. Using SNP data from genome-wide studies, we imputed and tested classical alleles and amino acid polymorphisms in 8 classical human leukocyte antigen (HLA) genes in 5,091 cases and 9,595 controls. We identified 11 statistically independent effects overall: 6 HLA-DRB1 and one DPB1 alleles in class II, one HLA-A and two B alleles in class I, and one signal in a region spanning from MICB to LST1. This genomic segment does not contain any HLA class I or II genes and provides robust evidence for the involvement of a non-HLA risk allele within the MHC. Interestingly, this region contains the TNF gene, the cognate ligand of the well-validated TNFRSF1A MS susceptibility gene. The classical HLA effects can be explained to some extent by polymorphic amino acid positions in the peptide-binding grooves. This study dissects the independent effects in the MHC, a critical region for MS susceptibility that harbors multiple risk alleles.</description><subject>Alleles</subject><subject>Amino acids</subject><subject>Biomedical research</subject><subject>Chromosome Mapping</subject><subject>Councils</subject><subject>Genetic aspects</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic screening</subject><subject>Genome-Wide Association Study</subject><subject>Genomes</subject><subject>Haplotypes</subject><subject>Health aspects</subject><subject>Histocompatibility antigens</subject><subject>Histocompatibility Antigens Class I - genetics</subject><subject>HLA histocompatibility antigens</subject><subject>HLA-DP beta-Chains - genetics</subject><subject>HLA-DRB1 Chains - genetics</subject><subject>Humans</subject><subject>Intracellular Signaling Peptides and Proteins</subject><subject>Linkage Disequilibrium</subject><subject>Major histocompatibility complex</subject><subject>Major Histocompatibility Complex - genetics</subject><subject>Medical research</subject><subject>Membrane Proteins - genetics</subject><subject>Methods</subject><subject>Multiple sclerosis</subject><subject>Multiple Sclerosis - genetics</subject><subject>Multiple Sclerosis - pathology</subject><subject>Physiological aspects</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Receptors, Tumor Necrosis Factor, Type I - genetics</subject><subject>Studies</subject><issn>1553-7404</issn><issn>1553-7390</issn><issn>1553-7404</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><sourceid>DOA</sourceid><recordid>eNqVk01v1DAQhiMEoqXwDxBEQkJwyGLHdj44IFUVpZVWVOLrajnOeNeLY4fYgVb8eZzdbbWROIByyIznmdfjsSdJnmK0wKTEbzZuHKwwi34FdoERInVe3EuOMWMkKymi9w_so-SR95vIsKouHyZHOc3LCuXlcfL7XFvIOtH32q7SsIY0ykHQMhXeO6lF0M6mTm1Dndi4IV1rH5x0XR9jjTY63KSTZ-A61TbtRhN0dFIvDQzOa_82vViepsK2qXU2m2xQCmTwj5MHShgPT_b_k-Tr-fsvZxfZ8urD5dnpMpOxxpAVmBCCRU2lQDRvVPSlbBuG25aVSBWUlbRqGcIK1xWUCIkGVJlT3BLARTz0SfJ8p9sb5_m-b55jWlSszlFdR-JyR7RObHg_6E4MN9wJzbcLblhxMcSmGOAFUCjaAsqKKUpqXIFiTFY5agpoFFZRK9tp-V_Qj81Mbb_0PVrAWc4InvZ-t69ubDpoJdgwCDNLm0esXvOV-8lJRYpyW_yrvcDgfozgA--0l2CMsODG7TlzXBXxziP6YoeuRDyKtspFRTnh_JTEahCjdOrX4i9U_FrotHQWlI7rs4TXs4TIBLgOKzF6zy8_f_oP9uO_s1ff5uzLA3YNwoS1d2ac3q-fg3QHyvg6_QDqrtUY8Wmybl8InyaL7ycrpj07vKa7pNtRIn8AATQegQ</recordid><startdate>20131101</startdate><enddate>20131101</enddate><creator>Patsopoulos, Nikolaos A</creator><creator>Barcellos, Lisa F</creator><creator>Hintzen, Rogier Q</creator><creator>Schaefer, Catherine</creator><creator>van Duijn, Cornelia M</creator><creator>Noble, Janelle A</creator><creator>Raj, Towfique</creator><creator>Gourraud, Pierre-Antoine</creator><creator>Stranger, Barbara E</creator><creator>Oksenberg, Jorge</creator><creator>Olsson, Tomas</creator><creator>Taylor, Bruce V</creator><creator>Sawcer, Stephen</creator><creator>Hafler, David A</creator><creator>Carrington, Mary</creator><creator>De Jager, Philip L</creator><creator>de Bakker, Paul I W</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>IOV</scope><scope>ISN</scope><scope>ISR</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope><scope>DOA</scope></search><sort><creationdate>20131101</creationdate><title>Fine-mapping the genetic association of the major histocompatibility complex in multiple sclerosis: HLA and non-HLA effects</title><author>Patsopoulos, Nikolaos A ; Barcellos, Lisa F ; Hintzen, Rogier Q ; Schaefer, Catherine ; van Duijn, Cornelia M ; Noble, Janelle A ; Raj, Towfique ; Gourraud, Pierre-Antoine ; Stranger, Barbara E ; Oksenberg, Jorge ; Olsson, Tomas ; Taylor, Bruce V ; Sawcer, Stephen ; Hafler, David A ; Carrington, Mary ; De Jager, Philip L ; de Bakker, Paul I W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c802t-613331a94ca042bf613ccdb51dd570f645748d501f198e700abef7241d3e16003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alleles</topic><topic>Amino acids</topic><topic>Biomedical research</topic><topic>Chromosome Mapping</topic><topic>Councils</topic><topic>Genetic aspects</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic screening</topic><topic>Genome-Wide Association Study</topic><topic>Genomes</topic><topic>Haplotypes</topic><topic>Health aspects</topic><topic>Histocompatibility antigens</topic><topic>Histocompatibility Antigens Class I - genetics</topic><topic>HLA histocompatibility antigens</topic><topic>HLA-DP beta-Chains - genetics</topic><topic>HLA-DRB1 Chains - genetics</topic><topic>Humans</topic><topic>Intracellular Signaling Peptides and Proteins</topic><topic>Linkage Disequilibrium</topic><topic>Major histocompatibility complex</topic><topic>Major Histocompatibility Complex - genetics</topic><topic>Medical research</topic><topic>Membrane Proteins - genetics</topic><topic>Methods</topic><topic>Multiple sclerosis</topic><topic>Multiple Sclerosis - genetics</topic><topic>Multiple Sclerosis - pathology</topic><topic>Physiological aspects</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Receptors, Tumor Necrosis Factor, Type I - genetics</topic><topic>Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Patsopoulos, Nikolaos A</creatorcontrib><creatorcontrib>Barcellos, Lisa F</creatorcontrib><creatorcontrib>Hintzen, Rogier Q</creatorcontrib><creatorcontrib>Schaefer, Catherine</creatorcontrib><creatorcontrib>van Duijn, Cornelia M</creatorcontrib><creatorcontrib>Noble, Janelle A</creatorcontrib><creatorcontrib>Raj, Towfique</creatorcontrib><creatorcontrib>Gourraud, Pierre-Antoine</creatorcontrib><creatorcontrib>Stranger, Barbara E</creatorcontrib><creatorcontrib>Oksenberg, Jorge</creatorcontrib><creatorcontrib>Olsson, Tomas</creatorcontrib><creatorcontrib>Taylor, Bruce V</creatorcontrib><creatorcontrib>Sawcer, Stephen</creatorcontrib><creatorcontrib>Hafler, David A</creatorcontrib><creatorcontrib>Carrington, Mary</creatorcontrib><creatorcontrib>De Jager, Philip L</creatorcontrib><creatorcontrib>de Bakker, Paul I W</creatorcontrib><creatorcontrib>IMSGC</creatorcontrib><creatorcontrib>ANZgene</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PLoS genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Patsopoulos, Nikolaos A</au><au>Barcellos, Lisa F</au><au>Hintzen, Rogier Q</au><au>Schaefer, Catherine</au><au>van Duijn, Cornelia M</au><au>Noble, Janelle A</au><au>Raj, Towfique</au><au>Gourraud, Pierre-Antoine</au><au>Stranger, Barbara E</au><au>Oksenberg, Jorge</au><au>Olsson, Tomas</au><au>Taylor, Bruce V</au><au>Sawcer, Stephen</au><au>Hafler, David A</au><au>Carrington, Mary</au><au>De Jager, Philip L</au><au>de Bakker, Paul I W</au><au>Gibson, Greg</au><aucorp>IMSGC</aucorp><aucorp>ANZgene</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fine-mapping the genetic association of the major histocompatibility complex in multiple sclerosis: HLA and non-HLA effects</atitle><jtitle>PLoS genetics</jtitle><addtitle>PLoS Genet</addtitle><date>2013-11-01</date><risdate>2013</risdate><volume>9</volume><issue>11</issue><spage>e1003926</spage><pages>e1003926-</pages><issn>1553-7404</issn><issn>1553-7390</issn><eissn>1553-7404</eissn><abstract>The major histocompatibility complex (MHC) region is strongly associated with multiple sclerosis (MS) susceptibility. HLA-DRB1*15:01 has the strongest effect, and several other alleles have been reported at different levels of validation. Using SNP data from genome-wide studies, we imputed and tested classical alleles and amino acid polymorphisms in 8 classical human leukocyte antigen (HLA) genes in 5,091 cases and 9,595 controls. We identified 11 statistically independent effects overall: 6 HLA-DRB1 and one DPB1 alleles in class II, one HLA-A and two B alleles in class I, and one signal in a region spanning from MICB to LST1. This genomic segment does not contain any HLA class I or II genes and provides robust evidence for the involvement of a non-HLA risk allele within the MHC. Interestingly, this region contains the TNF gene, the cognate ligand of the well-validated TNFRSF1A MS susceptibility gene. The classical HLA effects can be explained to some extent by polymorphic amino acid positions in the peptide-binding grooves. This study dissects the independent effects in the MHC, a critical region for MS susceptibility that harbors multiple risk alleles.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24278027</pmid><doi>10.1371/journal.pgen.1003926</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Alleles Amino acids Biomedical research Chromosome Mapping Councils Genetic aspects Genetic Predisposition to Disease Genetic screening Genome-Wide Association Study Genomes Haplotypes Health aspects Histocompatibility antigens Histocompatibility Antigens Class I - genetics HLA histocompatibility antigens HLA-DP beta-Chains - genetics HLA-DRB1 Chains - genetics Humans Intracellular Signaling Peptides and Proteins Linkage Disequilibrium Major histocompatibility complex Major Histocompatibility Complex - genetics Medical research Membrane Proteins - genetics Methods Multiple sclerosis Multiple Sclerosis - genetics Multiple Sclerosis - pathology Physiological aspects Polymorphism, Single Nucleotide Receptors, Tumor Necrosis Factor, Type I - genetics Studies |
| title | Fine-mapping the genetic association of the major histocompatibility complex in multiple sclerosis: HLA and non-HLA effects |
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