Autoantibody epitopes to the smaller isoform of glutamate decarboxylase do not differ in Swedish and Japanese type 1 diabetes patients and may be associated with high-risk human leucocyte antigen class II alleles
Type 1 diabetes (T1D) is an autoimmune disease with a strong human leucocyte antigen (HLA) class II association. Depending on geographic locations, the disease-associated HLA class II alleles vary. We evaluated the β cell-specific autoimmunity reflected in autoantibodies directed to the smaller isof...
Gespeichert in:
| Veröffentlicht in: | Clinical and experimental immunology 2007-12, Vol.150 (3), p.416-421 |
|---|---|
| Hauptverfasser: | , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 421 |
|---|---|
| container_issue | 3 |
| container_start_page | 416 |
| container_title | Clinical and experimental immunology |
| container_volume | 150 |
| creator | Maruyama, T Oak, S Hall, T.R Banga, J.P Ortqvist, E Ettinger, R.A Endl, J Hampe, C.S |
| description | Type 1 diabetes (T1D) is an autoimmune disease with a strong human leucocyte antigen (HLA) class II association. Depending on geographic locations, the disease-associated HLA class II alleles vary. We evaluated the β cell-specific autoimmunity reflected in autoantibodies directed to the smaller isoform of glutamate decarboxylase (GAD65) in Japanese and Swedish T1D patients. GAD65Ab epitope specificities were assessed using GAD65-specific recombinant Fab. GAD65Ab epitope specificities did not differ between Swedish and Japanese patients. Only recognition of the MICA-4-defined middle epitope was significantly stronger in the Japanese T1D patient group compared to the Swedish T1D patients (P = 0·001). Binding to the b96·11-defined middle epitope was substantial in both groups and showed significant associations with high-risk HLA class II haplotypes. In the Japanese T1D group the association was with haplotype DRB1*0802-DQB1*0302 (P = 0·0008), while in the Swedish T1D patients binding to the b96·11-defined epitope as associated with the presence of high-risk HLA genotypes DR3-DQB1*0201 and/or DR4-DQB1*0302 (P = 0·02). A significant association between reduction in binding in the presence of recombinant Fab (rFab) DPD and high-risk allele DQB1*0201 was found (P = 0·008) in the Swedish T1D patients only. We hypothesize that epitope-specific autoantibodies effect the peptide presentation on HLA class II molecules by modulating antigen uptake and processing. Molecular modelling of the high-risk HLA class II molecules will be necessary to test whether these different molecules present similar peptide-binding specificities. |
| doi_str_mv | 10.1111/j.1365-2249.2007.03527.x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_swepu</sourceid><recordid>TN_cdi_swepub_primary_oai_swepub_ki_se_567632</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>68503910</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5957-1abc2b7934717e836825a42ab72fb5f434e6778574af049f71c5715ed8a540053</originalsourceid><addsrcrecordid>eNqNks1u1DAUhSMEomXgFcAb2GWwnThOFiBVVYFBlViUrq0b52biaRKH2Ok078kD4XRGLV2BN_6537GP7RNFhNE1C-3jbs2STMScp8WaUyrXNBFcru-eRacPhefRKaW0iAtG05PolXO7MM2yjL-MTpgsRCZkcRr9Ppu8hd6b0lYzwcF4O6Aj3hLfIHEdtC2OxDhb27EjtibbdvLQgUdSoYaxtHdzCy7MLOmtJ5Wp60XQk6s9VsY1BPqKfIcBegyUnwckLFBQog_nDOAN9t7dUx3MpEQCzlltwgkV2RvfkMZsm3g07oY0Uwc9aXHSVs_BweJ7iz3RwYEjmw1Z3LboXkcvamgdvjn2q-j6y8XP82_x5Y-vm_Ozy1iLQsiYQal5KYsklUxinmQ5F5ByKCWvS1GnSYqZlLmQKdQ0LWrJtJBMYJWDSCkVySqKD_u6PQ5TqYbRdDDOyoJRx6WbMEIlMpklPPCfD3yodFjpcPMR2ieyp5XeNGprbxXnrEiC0VX04bjBaH9N6LzqjNPYtuF17eRUlguahA__J8ipoCLPFzA_gHq0zo1YP7hhVC1ZUzu1REotkVJL1tR91tRdkL79-zaPwmO4AvD-CIDT0NYj9Nq4R67Is4LmC_fpwO1Ni_N_G1DnF5tlFPTvDvoarIJtiIq6vuKUJZSGH2W5SP4A1Ob-bA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20505880</pqid></control><display><type>article</type><title>Autoantibody epitopes to the smaller isoform of glutamate decarboxylase do not differ in Swedish and Japanese type 1 diabetes patients and may be associated with high-risk human leucocyte antigen class II alleles</title><source>MEDLINE</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><source>SWEPUB Freely available online</source><source>EZB Electronic Journals Library</source><source>Oxford Journals</source><creator>Maruyama, T ; Oak, S ; Hall, T.R ; Banga, J.P ; Ortqvist, E ; Ettinger, R.A ; Endl, J ; Hampe, C.S</creator><creatorcontrib>Maruyama, T ; Oak, S ; Hall, T.R ; Banga, J.P ; Ortqvist, E ; Ettinger, R.A ; Endl, J ; Hampe, C.S</creatorcontrib><description>Type 1 diabetes (T1D) is an autoimmune disease with a strong human leucocyte antigen (HLA) class II association. Depending on geographic locations, the disease-associated HLA class II alleles vary. We evaluated the β cell-specific autoimmunity reflected in autoantibodies directed to the smaller isoform of glutamate decarboxylase (GAD65) in Japanese and Swedish T1D patients. GAD65Ab epitope specificities were assessed using GAD65-specific recombinant Fab. GAD65Ab epitope specificities did not differ between Swedish and Japanese patients. Only recognition of the MICA-4-defined middle epitope was significantly stronger in the Japanese T1D patient group compared to the Swedish T1D patients (P = 0·001). Binding to the b96·11-defined middle epitope was substantial in both groups and showed significant associations with high-risk HLA class II haplotypes. In the Japanese T1D group the association was with haplotype DRB1*0802-DQB1*0302 (P = 0·0008), while in the Swedish T1D patients binding to the b96·11-defined epitope as associated with the presence of high-risk HLA genotypes DR3-DQB1*0201 and/or DR4-DQB1*0302 (P = 0·02). A significant association between reduction in binding in the presence of recombinant Fab (rFab) DPD and high-risk allele DQB1*0201 was found (P = 0·008) in the Swedish T1D patients only. We hypothesize that epitope-specific autoantibodies effect the peptide presentation on HLA class II molecules by modulating antigen uptake and processing. Molecular modelling of the high-risk HLA class II molecules will be necessary to test whether these different molecules present similar peptide-binding specificities.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/j.1365-2249.2007.03527.x</identifier><identifier>PMID: 17956579</identifier><identifier>CODEN: CEXIAL</identifier><language>eng</language><publisher>Oxford, UK: Oxford, UK : Blackwell Publishing Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Alleles ; Analytical, structural and metabolic biochemistry ; Asian Continental Ancestry Group - genetics ; Autoantibodies - blood ; autoimmune ; Autoimmunity - genetics ; Biological and medical sciences ; Child ; Child, Preschool ; Diabetes Mellitus, Type 1 - ethnology ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Epitopes - genetics ; European Continental Ancestry Group - genetics ; Fundamental and applied biological sciences. Psychology ; GAD65 ; Genetic Predisposition to Disease ; Glutamate Decarboxylase - immunology ; HLA ; HLA-DR Antigens - genetics ; HLA-DRB1 Chains ; Humans ; Infant ; Infant, Newborn ; Isoenzymes - immunology ; Middle Aged ; Molecular and cellular biology ; Molecular biophysics ; RBA ; T1D ; Time Factors ; Translational Studies</subject><ispartof>Clinical and experimental immunology, 2007-12, Vol.150 (3), p.416-421</ispartof><rights>2008 INIST-CNRS</rights><rights>2007 The Author(s) Journal compilation © 2007 British Society for Immunology 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5957-1abc2b7934717e836825a42ab72fb5f434e6778574af049f71c5715ed8a540053</citedby><cites>FETCH-LOGICAL-c5957-1abc2b7934717e836825a42ab72fb5f434e6778574af049f71c5715ed8a540053</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/PMC2219379/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2219379/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,552,727,780,784,885,27915,27916,53782,53784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19869089$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17956579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:116195971$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Maruyama, T</creatorcontrib><creatorcontrib>Oak, S</creatorcontrib><creatorcontrib>Hall, T.R</creatorcontrib><creatorcontrib>Banga, J.P</creatorcontrib><creatorcontrib>Ortqvist, E</creatorcontrib><creatorcontrib>Ettinger, R.A</creatorcontrib><creatorcontrib>Endl, J</creatorcontrib><creatorcontrib>Hampe, C.S</creatorcontrib><title>Autoantibody epitopes to the smaller isoform of glutamate decarboxylase do not differ in Swedish and Japanese type 1 diabetes patients and may be associated with high-risk human leucocyte antigen class II alleles</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Type 1 diabetes (T1D) is an autoimmune disease with a strong human leucocyte antigen (HLA) class II association. Depending on geographic locations, the disease-associated HLA class II alleles vary. We evaluated the β cell-specific autoimmunity reflected in autoantibodies directed to the smaller isoform of glutamate decarboxylase (GAD65) in Japanese and Swedish T1D patients. GAD65Ab epitope specificities were assessed using GAD65-specific recombinant Fab. GAD65Ab epitope specificities did not differ between Swedish and Japanese patients. Only recognition of the MICA-4-defined middle epitope was significantly stronger in the Japanese T1D patient group compared to the Swedish T1D patients (P = 0·001). Binding to the b96·11-defined middle epitope was substantial in both groups and showed significant associations with high-risk HLA class II haplotypes. In the Japanese T1D group the association was with haplotype DRB1*0802-DQB1*0302 (P = 0·0008), while in the Swedish T1D patients binding to the b96·11-defined epitope as associated with the presence of high-risk HLA genotypes DR3-DQB1*0201 and/or DR4-DQB1*0302 (P = 0·02). A significant association between reduction in binding in the presence of recombinant Fab (rFab) DPD and high-risk allele DQB1*0201 was found (P = 0·008) in the Swedish T1D patients only. We hypothesize that epitope-specific autoantibodies effect the peptide presentation on HLA class II molecules by modulating antigen uptake and processing. Molecular modelling of the high-risk HLA class II molecules will be necessary to test whether these different molecules present similar peptide-binding specificities.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Alleles</subject><subject>Analytical, structural and metabolic biochemistry</subject><subject>Asian Continental Ancestry Group - genetics</subject><subject>Autoantibodies - blood</subject><subject>autoimmune</subject><subject>Autoimmunity - genetics</subject><subject>Biological and medical sciences</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Diabetes Mellitus, Type 1 - ethnology</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Epitopes - genetics</subject><subject>European Continental Ancestry Group - genetics</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GAD65</subject><subject>Genetic Predisposition to Disease</subject><subject>Glutamate Decarboxylase - immunology</subject><subject>HLA</subject><subject>HLA-DR Antigens - genetics</subject><subject>HLA-DRB1 Chains</subject><subject>Humans</subject><subject>Infant</subject><subject>Infant, Newborn</subject><subject>Isoenzymes - immunology</subject><subject>Middle Aged</subject><subject>Molecular and cellular biology</subject><subject>Molecular biophysics</subject><subject>RBA</subject><subject>T1D</subject><subject>Time Factors</subject><subject>Translational Studies</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNqNks1u1DAUhSMEomXgFcAb2GWwnThOFiBVVYFBlViUrq0b52biaRKH2Ok078kD4XRGLV2BN_6537GP7RNFhNE1C-3jbs2STMScp8WaUyrXNBFcru-eRacPhefRKaW0iAtG05PolXO7MM2yjL-MTpgsRCZkcRr9Ppu8hd6b0lYzwcF4O6Aj3hLfIHEdtC2OxDhb27EjtibbdvLQgUdSoYaxtHdzCy7MLOmtJ5Wp60XQk6s9VsY1BPqKfIcBegyUnwckLFBQog_nDOAN9t7dUx3MpEQCzlltwgkV2RvfkMZsm3g07oY0Uwc9aXHSVs_BweJ7iz3RwYEjmw1Z3LboXkcvamgdvjn2q-j6y8XP82_x5Y-vm_Ozy1iLQsiYQal5KYsklUxinmQ5F5ByKCWvS1GnSYqZlLmQKdQ0LWrJtJBMYJWDSCkVySqKD_u6PQ5TqYbRdDDOyoJRx6WbMEIlMpklPPCfD3yodFjpcPMR2ieyp5XeNGprbxXnrEiC0VX04bjBaH9N6LzqjNPYtuF17eRUlguahA__J8ipoCLPFzA_gHq0zo1YP7hhVC1ZUzu1REotkVJL1tR91tRdkL79-zaPwmO4AvD-CIDT0NYj9Nq4R67Is4LmC_fpwO1Ni_N_G1DnF5tlFPTvDvoarIJtiIq6vuKUJZSGH2W5SP4A1Ob-bA</recordid><startdate>200712</startdate><enddate>200712</enddate><creator>Maruyama, T</creator><creator>Oak, S</creator><creator>Hall, T.R</creator><creator>Banga, J.P</creator><creator>Ortqvist, E</creator><creator>Ettinger, R.A</creator><creator>Endl, J</creator><creator>Hampe, C.S</creator><general>Oxford, UK : Blackwell Publishing Ltd</general><general>Blackwell Publishing Ltd</general><general>Blackwell</general><general>Blackwell Science Inc</general><scope>FBQ</scope><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>7T5</scope><scope>H94</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>200712</creationdate><title>Autoantibody epitopes to the smaller isoform of glutamate decarboxylase do not differ in Swedish and Japanese type 1 diabetes patients and may be associated with high-risk human leucocyte antigen class II alleles</title><author>Maruyama, T ; Oak, S ; Hall, T.R ; Banga, J.P ; Ortqvist, E ; Ettinger, R.A ; Endl, J ; Hampe, C.S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5957-1abc2b7934717e836825a42ab72fb5f434e6778574af049f71c5715ed8a540053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Alleles</topic><topic>Analytical, structural and metabolic biochemistry</topic><topic>Asian Continental Ancestry Group - genetics</topic><topic>Autoantibodies - blood</topic><topic>autoimmune</topic><topic>Autoimmunity - genetics</topic><topic>Biological and medical sciences</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Diabetes Mellitus, Type 1 - ethnology</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Epitopes - genetics</topic><topic>European Continental Ancestry Group - genetics</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GAD65</topic><topic>Genetic Predisposition to Disease</topic><topic>Glutamate Decarboxylase - immunology</topic><topic>HLA</topic><topic>HLA-DR Antigens - genetics</topic><topic>HLA-DRB1 Chains</topic><topic>Humans</topic><topic>Infant</topic><topic>Infant, Newborn</topic><topic>Isoenzymes - immunology</topic><topic>Middle Aged</topic><topic>Molecular and cellular biology</topic><topic>Molecular biophysics</topic><topic>RBA</topic><topic>T1D</topic><topic>Time Factors</topic><topic>Translational Studies</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maruyama, T</creatorcontrib><creatorcontrib>Oak, S</creatorcontrib><creatorcontrib>Hall, T.R</creatorcontrib><creatorcontrib>Banga, J.P</creatorcontrib><creatorcontrib>Ortqvist, E</creatorcontrib><creatorcontrib>Ettinger, R.A</creatorcontrib><creatorcontrib>Endl, J</creatorcontrib><creatorcontrib>Hampe, C.S</creatorcontrib><collection>AGRIS</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>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</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><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maruyama, T</au><au>Oak, S</au><au>Hall, T.R</au><au>Banga, J.P</au><au>Ortqvist, E</au><au>Ettinger, R.A</au><au>Endl, J</au><au>Hampe, C.S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Autoantibody epitopes to the smaller isoform of glutamate decarboxylase do not differ in Swedish and Japanese type 1 diabetes patients and may be associated with high-risk human leucocyte antigen class II alleles</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2007-12</date><risdate>2007</risdate><volume>150</volume><issue>3</issue><spage>416</spage><epage>421</epage><pages>416-421</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><coden>CEXIAL</coden><abstract>Type 1 diabetes (T1D) is an autoimmune disease with a strong human leucocyte antigen (HLA) class II association. Depending on geographic locations, the disease-associated HLA class II alleles vary. We evaluated the β cell-specific autoimmunity reflected in autoantibodies directed to the smaller isoform of glutamate decarboxylase (GAD65) in Japanese and Swedish T1D patients. GAD65Ab epitope specificities were assessed using GAD65-specific recombinant Fab. GAD65Ab epitope specificities did not differ between Swedish and Japanese patients. Only recognition of the MICA-4-defined middle epitope was significantly stronger in the Japanese T1D patient group compared to the Swedish T1D patients (P = 0·001). Binding to the b96·11-defined middle epitope was substantial in both groups and showed significant associations with high-risk HLA class II haplotypes. In the Japanese T1D group the association was with haplotype DRB1*0802-DQB1*0302 (P = 0·0008), while in the Swedish T1D patients binding to the b96·11-defined epitope as associated with the presence of high-risk HLA genotypes DR3-DQB1*0201 and/or DR4-DQB1*0302 (P = 0·02). A significant association between reduction in binding in the presence of recombinant Fab (rFab) DPD and high-risk allele DQB1*0201 was found (P = 0·008) in the Swedish T1D patients only. We hypothesize that epitope-specific autoantibodies effect the peptide presentation on HLA class II molecules by modulating antigen uptake and processing. Molecular modelling of the high-risk HLA class II molecules will be necessary to test whether these different molecules present similar peptide-binding specificities.</abstract><cop>Oxford, UK</cop><pub>Oxford, UK : Blackwell Publishing Ltd</pub><pmid>17956579</pmid><doi>10.1111/j.1365-2249.2007.03527.x</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0009-9104 |
| ispartof | Clinical and experimental immunology, 2007-12, Vol.150 (3), p.416-421 |
| issn | 0009-9104 1365-2249 |
| language | eng |
| recordid | cdi_swepub_primary_oai_swepub_ki_se_567632 |
| source | MEDLINE; PubMed Central; Alma/SFX Local Collection; SWEPUB Freely available online; EZB Electronic Journals Library; Oxford Journals |
| subjects | Adolescent Adult Aged Aged, 80 and over Alleles Analytical, structural and metabolic biochemistry Asian Continental Ancestry Group - genetics Autoantibodies - blood autoimmune Autoimmunity - genetics Biological and medical sciences Child Child, Preschool Diabetes Mellitus, Type 1 - ethnology Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Epitopes - genetics European Continental Ancestry Group - genetics Fundamental and applied biological sciences. Psychology GAD65 Genetic Predisposition to Disease Glutamate Decarboxylase - immunology HLA HLA-DR Antigens - genetics HLA-DRB1 Chains Humans Infant Infant, Newborn Isoenzymes - immunology Middle Aged Molecular and cellular biology Molecular biophysics RBA T1D Time Factors Translational Studies |
| title | Autoantibody epitopes to the smaller isoform of glutamate decarboxylase do not differ in Swedish and Japanese type 1 diabetes patients and may be associated with high-risk human leucocyte antigen class II alleles |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T18%3A17%3A56IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_swepu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Autoantibody%20epitopes%20to%20the%20smaller%20isoform%20of%20glutamate%20decarboxylase%20do%20not%20differ%20in%20Swedish%20and%20Japanese%20type%201%20diabetes%20patients%20and%20may%20be%20associated%20with%20high-risk%20human%20leucocyte%20antigen%20class%20II%20alleles&rft.jtitle=Clinical%20and%20experimental%20immunology&rft.au=Maruyama,%20T&rft.date=2007-12&rft.volume=150&rft.issue=3&rft.spage=416&rft.epage=421&rft.pages=416-421&rft.issn=0009-9104&rft.eissn=1365-2249&rft.coden=CEXIAL&rft_id=info:doi/10.1111/j.1365-2249.2007.03527.x&rft_dat=%3Cproquest_swepu%3E68503910%3C/proquest_swepu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=20505880&rft_id=info:pmid/17956579&rfr_iscdi=true |