Association of HLA-DM polymorphism with the production of antiphospholipid antibodies

Objective: To investigate whether variation in the HLA-DM gene is important in producing a group of pathogenic autoantibodies—antiphospholipid antibodies (aPL)—on the basis that HLA class II restricted antigen presentation is involved in the production of aPL. Methods: HLA-DMA and DMB polymorphisms...

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Veröffentlicht in:Annals of the rheumatic diseases 2004-12, Vol.63 (12), p.1645-1648
Hauptverfasser: Sanchez, M L, Katsumata, K, Atsumi, T, Romero, F I, Bertolaccini, M L, Funke, A, Amengual, O, Kondeatis, E, Vaughan, R W, Cox, A, Hughes, G R V, Khamashta, M A
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container_end_page 1648
container_issue 12
container_start_page 1645
container_title Annals of the rheumatic diseases
container_volume 63
creator Sanchez, M L
Katsumata, K
Atsumi, T
Romero, F I
Bertolaccini, M L
Funke, A
Amengual, O
Kondeatis, E
Vaughan, R W
Cox, A
Hughes, G R V
Khamashta, M A
description Objective: To investigate whether variation in the HLA-DM gene is important in producing a group of pathogenic autoantibodies—antiphospholipid antibodies (aPL)—on the basis that HLA class II restricted antigen presentation is involved in the production of aPL. Methods: HLA-DMA and DMB polymorphisms were genotyped by polymerase chain reaction combined with restriction enzyme digestion in 51 white patients with primary antiphospholipid syndrome (APS), 82 with systemic lupus erythematosus (SLE) (42 with APS and 40 without APS), and 109 healthy white controls. The association with the aPL profile was examined. Results: The distribution of DMA alleles in APS patients and in patients with APS associated with SLE was significantly different from that in controls by 4×2 χ2 test with 3 degrees of freedom (p = 0.035 and 0.011, respectively), but it was not different between SLE patients without APS and controls. The allelic distribution of DMA was also different between patients with IgG class anticardiolipin antibody or those with lupus anticoagulant (LA) and controls (p = 0.012 and 0.007, respectively) and between patients with and without LA among SLE patients (p = 0.035). All these differences included the increase in DMA*0102 in the former groups. Conclusions: The results suggest that HLA-DMA*0102 or its linked gene(s) form one of the genetic risks for the production of aPL.
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All these differences included the increase in DMA*0102 in the former groups. Conclusions: The results suggest that HLA-DMA*0102 or its linked gene(s) form one of the genetic risks for the production of aPL.</description><identifier>ISSN: 0003-4967</identifier><identifier>EISSN: 1468-2060</identifier><identifier>DOI: 10.1136/ard.2003.015552</identifier><identifier>PMID: 15547089</identifier><identifier>CODEN: ARDIAO</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and European League Against Rheumatism</publisher><subject>Adult ; Aged ; Antibodies, Antiphospholipid - biosynthesis ; anticardiolipin antibody ; Anticoagulants ; Antigens ; antiphospholipid antibodies ; antiphospholipid antibody ; antiphospholipid syndrome ; Antiphospholipid Syndrome - etiology ; Antiphospholipid Syndrome - genetics ; aPL ; APS ; Biological and medical sciences ; Extended Report ; Female ; Gene Frequency ; Genes ; Genetic Predisposition to Disease ; Genotype ; Growth hormones ; Haplotypes ; Hematologic and hematopoietic diseases ; Histocompatibility Testing ; HLA-D Antigens - genetics ; HLA-DM ; Humans ; Lupus ; lupus anticoagulant ; Lupus Erythematosus, Systemic - complications ; Male ; Medical sciences ; Middle Aged ; Peptides ; Platelet diseases and coagulopathies ; Polymorphism, Genetic ; Population ; restriction fragment length polymorphism ; RFLP</subject><ispartof>Annals of the rheumatic diseases, 2004-12, Vol.63 (12), p.1645-1648</ispartof><rights>Copyright 2004 by Annals of the Rheumatic Diseases</rights><rights>2005 INIST-CNRS</rights><rights>Copyright: 2004 Copyright 2004 by Annals of the Rheumatic Diseases</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b520t-239f446c3346faa7e2266e18caad0b763dd3bebb93f863ffc3d55099546ba92f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1754864/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1754864/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=16324490$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15547089$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sanchez, M L</creatorcontrib><creatorcontrib>Katsumata, K</creatorcontrib><creatorcontrib>Atsumi, T</creatorcontrib><creatorcontrib>Romero, F I</creatorcontrib><creatorcontrib>Bertolaccini, M L</creatorcontrib><creatorcontrib>Funke, A</creatorcontrib><creatorcontrib>Amengual, O</creatorcontrib><creatorcontrib>Kondeatis, E</creatorcontrib><creatorcontrib>Vaughan, R W</creatorcontrib><creatorcontrib>Cox, A</creatorcontrib><creatorcontrib>Hughes, G R V</creatorcontrib><creatorcontrib>Khamashta, M A</creatorcontrib><title>Association of HLA-DM polymorphism with the production of antiphospholipid antibodies</title><title>Annals of the rheumatic diseases</title><addtitle>Ann Rheum Dis</addtitle><description>Objective: To investigate whether variation in the HLA-DM gene is important in producing a group of pathogenic autoantibodies—antiphospholipid antibodies (aPL)—on the basis that HLA class II restricted antigen presentation is involved in the production of aPL. Methods: HLA-DMA and DMB polymorphisms were genotyped by polymerase chain reaction combined with restriction enzyme digestion in 51 white patients with primary antiphospholipid syndrome (APS), 82 with systemic lupus erythematosus (SLE) (42 with APS and 40 without APS), and 109 healthy white controls. The association with the aPL profile was examined. Results: The distribution of DMA alleles in APS patients and in patients with APS associated with SLE was significantly different from that in controls by 4×2 χ2 test with 3 degrees of freedom (p = 0.035 and 0.011, respectively), but it was not different between SLE patients without APS and controls. The allelic distribution of DMA was also different between patients with IgG class anticardiolipin antibody or those with lupus anticoagulant (LA) and controls (p = 0.012 and 0.007, respectively) and between patients with and without LA among SLE patients (p = 0.035). All these differences included the increase in DMA*0102 in the former groups. 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Katsumata, K ; Atsumi, T ; Romero, F I ; Bertolaccini, M L ; Funke, A ; Amengual, O ; Kondeatis, E ; Vaughan, R W ; Cox, A ; Hughes, G R V ; Khamashta, M A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b520t-239f446c3346faa7e2266e18caad0b763dd3bebb93f863ffc3d55099546ba92f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antibodies, Antiphospholipid - biosynthesis</topic><topic>anticardiolipin antibody</topic><topic>Anticoagulants</topic><topic>Antigens</topic><topic>antiphospholipid antibodies</topic><topic>antiphospholipid antibody</topic><topic>antiphospholipid syndrome</topic><topic>Antiphospholipid Syndrome - etiology</topic><topic>Antiphospholipid Syndrome - genetics</topic><topic>aPL</topic><topic>APS</topic><topic>Biological and medical sciences</topic><topic>Extended Report</topic><topic>Female</topic><topic>Gene Frequency</topic><topic>Genes</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Growth hormones</topic><topic>Haplotypes</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Histocompatibility Testing</topic><topic>HLA-D Antigens - genetics</topic><topic>HLA-DM</topic><topic>Humans</topic><topic>Lupus</topic><topic>lupus anticoagulant</topic><topic>Lupus Erythematosus, Systemic - complications</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Peptides</topic><topic>Platelet diseases and coagulopathies</topic><topic>Polymorphism, Genetic</topic><topic>Population</topic><topic>restriction fragment length polymorphism</topic><topic>RFLP</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sanchez, M L</creatorcontrib><creatorcontrib>Katsumata, K</creatorcontrib><creatorcontrib>Atsumi, T</creatorcontrib><creatorcontrib>Romero, F I</creatorcontrib><creatorcontrib>Bertolaccini, M L</creatorcontrib><creatorcontrib>Funke, A</creatorcontrib><creatorcontrib>Amengual, O</creatorcontrib><creatorcontrib>Kondeatis, E</creatorcontrib><creatorcontrib>Vaughan, R W</creatorcontrib><creatorcontrib>Cox, A</creatorcontrib><creatorcontrib>Hughes, G R V</creatorcontrib><creatorcontrib>Khamashta, M A</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health &amp; 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Methods: HLA-DMA and DMB polymorphisms were genotyped by polymerase chain reaction combined with restriction enzyme digestion in 51 white patients with primary antiphospholipid syndrome (APS), 82 with systemic lupus erythematosus (SLE) (42 with APS and 40 without APS), and 109 healthy white controls. The association with the aPL profile was examined. Results: The distribution of DMA alleles in APS patients and in patients with APS associated with SLE was significantly different from that in controls by 4×2 χ2 test with 3 degrees of freedom (p = 0.035 and 0.011, respectively), but it was not different between SLE patients without APS and controls. The allelic distribution of DMA was also different between patients with IgG class anticardiolipin antibody or those with lupus anticoagulant (LA) and controls (p = 0.012 and 0.007, respectively) and between patients with and without LA among SLE patients (p = 0.035). All these differences included the increase in DMA*0102 in the former groups. Conclusions: The results suggest that HLA-DMA*0102 or its linked gene(s) form one of the genetic risks for the production of aPL.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and European League Against Rheumatism</pub><pmid>15547089</pmid><doi>10.1136/ard.2003.015552</doi><tpages>4</tpages><oa>free_for_read</oa></addata></record>
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ispartof Annals of the rheumatic diseases, 2004-12, Vol.63 (12), p.1645-1648
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subjects Adult
Aged
Antibodies, Antiphospholipid - biosynthesis
anticardiolipin antibody
Anticoagulants
Antigens
antiphospholipid antibodies
antiphospholipid antibody
antiphospholipid syndrome
Antiphospholipid Syndrome - etiology
Antiphospholipid Syndrome - genetics
aPL
APS
Biological and medical sciences
Extended Report
Female
Gene Frequency
Genes
Genetic Predisposition to Disease
Genotype
Growth hormones
Haplotypes
Hematologic and hematopoietic diseases
Histocompatibility Testing
HLA-D Antigens - genetics
HLA-DM
Humans
Lupus
lupus anticoagulant
Lupus Erythematosus, Systemic - complications
Male
Medical sciences
Middle Aged
Peptides
Platelet diseases and coagulopathies
Polymorphism, Genetic
Population
restriction fragment length polymorphism
RFLP
title Association of HLA-DM polymorphism with the production of antiphospholipid antibodies
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