Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis
Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3...
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Veröffentlicht in: | Neurology 2004-12, Vol.63 (12), p.2396-2398 |
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container_title | Neurology |
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description | Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. Patients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM. |
doi_str_mv | 10.1212/01.WNL.0000148588.15052.4C |
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A ; SCHREUDER, G. M. Th ; GIPHART, M. J ; GELEIJNS, K ; VERSCHUUREN, J. J. G. M ; WINTZEN, A. R</creator><creatorcontrib>BADRISING, U. A ; SCHREUDER, G. M. Th ; GIPHART, M. J ; GELEIJNS, K ; VERSCHUUREN, J. J. G. M ; WINTZEN, A. R ; Dutch IBM Study Group ; the Dutch IBM Study Group</creatorcontrib><description>Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. Patients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM.</description><identifier>ISSN: 0028-3878</identifier><identifier>EISSN: 1526-632X</identifier><identifier>DOI: 10.1212/01.WNL.0000148588.15052.4C</identifier><identifier>PMID: 15623710</identifier><identifier>CODEN: NEURAI</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Age of Onset ; Aged ; Aged, 80 and over ; Autoimmune Diseases - epidemiology ; Autoimmune Diseases - genetics ; Autoimmune Diseases - immunology ; Biological and medical sciences ; Comorbidity ; Diseases of striated muscles. Neuromuscular diseases ; Female ; Gene Frequency ; Genes, MHC Class I ; Genes, MHC Class II ; Genetic Predisposition to Disease ; Haplotypes - genetics ; HLA Antigens - analysis ; HLA Antigens - genetics ; HLA Antigens - immunology ; HLA-D Antigens - analysis ; HLA-D Antigens - genetics ; HLA-D Antigens - immunology ; HLA-DR Antigens - analysis ; HLA-DR Antigens - genetics ; HLA-DR Antigens - immunology ; HLA-DRB4 Chains ; Humans ; Male ; Medical sciences ; Middle Aged ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis ; Myositis, Inclusion Body - epidemiology ; Myositis, Inclusion Body - genetics ; Myositis, Inclusion Body - immunology ; Netherlands - epidemiology ; Neurology ; Prevalence</subject><ispartof>Neurology, 2004-12, Vol.63 (12), p.2396-2398</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-750b771b489af3cec42a92017cee8818c674296dd9c7ea02487da19725113c1f3</citedby><cites>FETCH-LOGICAL-c404t-750b771b489af3cec42a92017cee8818c674296dd9c7ea02487da19725113c1f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16387734$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15623710$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BADRISING, U. A</creatorcontrib><creatorcontrib>SCHREUDER, G. M. Th</creatorcontrib><creatorcontrib>GIPHART, M. J</creatorcontrib><creatorcontrib>GELEIJNS, K</creatorcontrib><creatorcontrib>VERSCHUUREN, J. J. G. M</creatorcontrib><creatorcontrib>WINTZEN, A. R</creatorcontrib><creatorcontrib>Dutch IBM Study Group</creatorcontrib><creatorcontrib>the Dutch IBM Study Group</creatorcontrib><title>Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis</title><title>Neurology</title><addtitle>Neurology</addtitle><description>Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. Patients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM.</description><subject>Age of Onset</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Autoimmune Diseases - epidemiology</subject><subject>Autoimmune Diseases - genetics</subject><subject>Autoimmune Diseases - immunology</subject><subject>Biological and medical sciences</subject><subject>Comorbidity</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Female</subject><subject>Gene Frequency</subject><subject>Genes, MHC Class I</subject><subject>Genes, MHC Class II</subject><subject>Genetic Predisposition to Disease</subject><subject>Haplotypes - genetics</subject><subject>HLA Antigens - analysis</subject><subject>HLA Antigens - genetics</subject><subject>HLA Antigens - immunology</subject><subject>HLA-D Antigens - analysis</subject><subject>HLA-D Antigens - genetics</subject><subject>HLA-D Antigens - immunology</subject><subject>HLA-DR Antigens - analysis</subject><subject>HLA-DR Antigens - genetics</subject><subject>HLA-DR Antigens - immunology</subject><subject>HLA-DRB4 Chains</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Myositis, Inclusion Body - epidemiology</subject><subject>Myositis, Inclusion Body - genetics</subject><subject>Myositis, Inclusion Body - immunology</subject><subject>Netherlands - epidemiology</subject><subject>Neurology</subject><subject>Prevalence</subject><issn>0028-3878</issn><issn>1526-632X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkV1LwzAUhoMoOqd_QYKgd605adqk3o3hx2DojaJ3IUtTjbSN9rTI_r3ZHCwEDoHnfQ88IeQSWAoc-A2D9O1pmbJ4QKhcqRRylvNUzA_IBHJeJEXG3w_JhDGukkxJdUJOEb8innNZHpMTyAueSWATYmaIwXoz-NAh_fXDJzXjEHzbjp2jlcfQV65HarqKPi5n1DYGkS6278VmDP7DxaTv4rXNiLGHrkK1pu06oB88npGj2jTozndzSl7v717mj8ny-WExny0TK5gYEpmzlZSwEqo0dWadFdyUnIG0zikFyhZS8LKoqtJKZxgXSlYGSslzgMxCnU3J9X_vdx9-RoeDbj1a1zSmc2FEXcjYVioWwdt_0PYBsXe1_u59a_q1BqY3gjUDHQXrvWC9FazFPIYvdlvGVeuqfXRnNAJXO8CgNU3dm8563HNF_A-ZiewPkJyEGQ</recordid><startdate>20041228</startdate><enddate>20041228</enddate><creator>BADRISING, U. A</creator><creator>SCHREUDER, G. M. Th</creator><creator>GIPHART, M. J</creator><creator>GELEIJNS, K</creator><creator>VERSCHUUREN, J. J. G. M</creator><creator>WINTZEN, A. R</creator><general>Lippincott Williams & Wilkins</general><scope>IQODW</scope><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>7X8</scope></search><sort><creationdate>20041228</creationdate><title>Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis</title><author>BADRISING, U. A ; SCHREUDER, G. M. Th ; GIPHART, M. J ; GELEIJNS, K ; VERSCHUUREN, J. J. G. M ; WINTZEN, A. 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Neuromuscular diseases</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genes, MHC Class I</topic><topic>Genes, MHC Class II</topic><topic>Genetic Predisposition to Disease</topic><topic>Haplotypes - genetics</topic><topic>HLA Antigens - analysis</topic><topic>HLA Antigens - genetics</topic><topic>HLA Antigens - immunology</topic><topic>HLA-D Antigens - analysis</topic><topic>HLA-D Antigens - genetics</topic><topic>HLA-D Antigens - immunology</topic><topic>HLA-DR Antigens - analysis</topic><topic>HLA-DR Antigens - genetics</topic><topic>HLA-DR Antigens - immunology</topic><topic>HLA-DRB4 Chains</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Myositis, Inclusion Body - epidemiology</topic><topic>Myositis, Inclusion Body - genetics</topic><topic>Myositis, Inclusion Body - immunology</topic><topic>Netherlands - epidemiology</topic><topic>Neurology</topic><topic>Prevalence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BADRISING, U. A</creatorcontrib><creatorcontrib>SCHREUDER, G. M. Th</creatorcontrib><creatorcontrib>GIPHART, M. J</creatorcontrib><creatorcontrib>GELEIJNS, K</creatorcontrib><creatorcontrib>VERSCHUUREN, J. J. G. M</creatorcontrib><creatorcontrib>WINTZEN, A. 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R</au><aucorp>Dutch IBM Study Group</aucorp><aucorp>the Dutch IBM Study Group</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis</atitle><jtitle>Neurology</jtitle><addtitle>Neurology</addtitle><date>2004-12-28</date><risdate>2004</risdate><volume>63</volume><issue>12</issue><spage>2396</spage><epage>2398</epage><pages>2396-2398</pages><issn>0028-3878</issn><eissn>1526-632X</eissn><coden>NEURAI</coden><abstract>Whether autoimmune mechanisms play a role in the pathogenesis of inclusion body myositis (IBM) is unknown. Human leukocyte antigen (HLA) analysis in 52 patients, including 17 with autoimmune disorders (AIDs), showed that patients were more likely to have antigens from the autoimmune-prone HLA-B8-DR3 ancestral haplotype than healthy control subjects, irrespective of the presence of AIDs. Patients lacked the apparently protective HLA-DR53 antigen. The results provide further support for an autoimmune basis in IBM.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>15623710</pmid><doi>10.1212/01.WNL.0000148588.15052.4C</doi><tpages>3</tpages></addata></record> |
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subjects | Age of Onset Aged Aged, 80 and over Autoimmune Diseases - epidemiology Autoimmune Diseases - genetics Autoimmune Diseases - immunology Biological and medical sciences Comorbidity Diseases of striated muscles. Neuromuscular diseases Female Gene Frequency Genes, MHC Class I Genes, MHC Class II Genetic Predisposition to Disease Haplotypes - genetics HLA Antigens - analysis HLA Antigens - genetics HLA Antigens - immunology HLA-D Antigens - analysis HLA-D Antigens - genetics HLA-D Antigens - immunology HLA-DR Antigens - analysis HLA-DR Antigens - genetics HLA-DR Antigens - immunology HLA-DRB4 Chains Humans Male Medical sciences Middle Aged Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis Myositis, Inclusion Body - epidemiology Myositis, Inclusion Body - genetics Myositis, Inclusion Body - immunology Netherlands - epidemiology Neurology Prevalence |
title | Associations with autoimmune disorders and HLA class I and II antigens in inclusion body myositis |
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