The association between the HLA-G 14-bp insertion/deletion polymorphism and type 1 diabetes
Type 1 diabetes (T1D) is a multifactorial disease that has a strong genetic component. The HLA-G is a nonclassical HLA class I locus that is associated with immunomodulatory functions, including downregulation of innate and adaptive immune responses and induction of immune tolerance. However, there...
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| Veröffentlicht in: | Genes and immunity 2016-01, Vol.17 (1), p.13-18 |
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| creator | Silva, H P V Ururahy, M A G Souza, K S C Loureiro, M B Oliveira, Y M C Oliveira, G H M Luchessi, A D Carvalho, K T C Freitas, J C O C Donadi, E A Hirata, R D C Almeida, M G Arrais, R F Hirata, M H Rezende, A A |
| description | Type 1 diabetes (T1D) is a multifactorial disease that has a strong genetic component. The
HLA-G
is a nonclassical
HLA
class I locus that is associated with immunomodulatory functions, including downregulation of innate and adaptive immune responses and induction of immune tolerance. However, there is currently limited information about the involvement of
HLA-G
in T1D susceptibility. This case-control study aims to investigate the T1D susceptibility association of alleles and genotypes of a widely investigated 14-bp insertion/deletion polymorphism in the
HLA-G
and to provide further evidence of the frequency distribution of class II
HLA-DR-DQ
-risk genotypes in T1D children and adolescents in the Brazilian population. The deletion allele and the homozygous deletion genotype are associated with susceptibility to T1D and the insertion allele and the heterozygous deletion/insertion genotype are associated with protection from T1D. We also confirm that genetic susceptibility to T1D is associated with the
DRB1*03:01-DQA1*05:01-DQB1*02:01
and
DRB1*04-DQA1*03:01-DQB1*03:02
haplotypes in Brazilian northeast region. The DR3-DQ2/DR4-DQ8 genotype conferred the highest detected risk for T1D. Our results identify a novel association of the 14-bp deletion allele and the homozygous deletion genotype with T1D development and provide additional evidence of the importance of
HLA
class II heterozygous DR3-DQ2/DR4-DQ8 genotype in T1D susceptibility. |
| doi_str_mv | 10.1038/gene.2015.45 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_1765981536</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A442535495</galeid><sourcerecordid>A442535495</sourcerecordid><originalsourceid>FETCH-LOGICAL-c690t-146e8dfb693ac22393d212399f8d085d6b88b23de79eb24183681b8507e119783</originalsourceid><addsrcrecordid>eNqN0s9rFDEUB_BBFFurN88y4EXB2eZNfkxyXIq2hQVB68lDyEzebKfMJGMyS93_3oxbdVdKlRwSkk--CY-XZS-BLIBQebpGh4uSAF8w_ig7BlaJgrOKPJ7XQhRMVuooexbjDSEgQKin2VEpmCo5qOPs69U15iZG33Rm6rzLa5xuEV0-pf2L1bI4z4EV9Zh3LmKYxanFHn_S0ffbwYfxuotDbpzNp-2IOeS2MykF4_PsSWv6iC_u5pPsy4f3V2cXxerj-eXZclU0QpGpSL9EadtaKGqasqSK2hLSpFppieRW1FLWJbVYKaxLBpIKCbXkpEIAVUl6kr3Z5Y7Bf9tgnPTQxQb73jj0m6ihElxJ4FQk-voveuM3waXf6VQTqKjgRD2koOKSKyYY_aPWpkfdudZPwTTz03qZYogQoNSDirGSU84UT2pxj0rD4tA13mHbpf2D2P-6sP_C24MLyUz4fVqbTYz68vOnw_B_2f3cdzvbBB9jwFaPoRtM2Gogem5QPTeonhtUs5m_uivtph7Q_sa_OjKBYgdiOnJrDHu1vy_wB5C758A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1758594643</pqid></control><display><type>article</type><title>The association between the HLA-G 14-bp insertion/deletion polymorphism and type 1 diabetes</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Silva, H P V ; Ururahy, M A G ; Souza, K S C ; Loureiro, M B ; Oliveira, Y M C ; Oliveira, G H M ; Luchessi, A D ; Carvalho, K T C ; Freitas, J C O C ; Donadi, E A ; Hirata, R D C ; Almeida, M G ; Arrais, R F ; Hirata, M H ; Rezende, A A</creator><creatorcontrib>Silva, H P V ; Ururahy, M A G ; Souza, K S C ; Loureiro, M B ; Oliveira, Y M C ; Oliveira, G H M ; Luchessi, A D ; Carvalho, K T C ; Freitas, J C O C ; Donadi, E A ; Hirata, R D C ; Almeida, M G ; Arrais, R F ; Hirata, M H ; Rezende, A A</creatorcontrib><description>Type 1 diabetes (T1D) is a multifactorial disease that has a strong genetic component. The
HLA-G
is a nonclassical
HLA
class I locus that is associated with immunomodulatory functions, including downregulation of innate and adaptive immune responses and induction of immune tolerance. However, there is currently limited information about the involvement of
HLA-G
in T1D susceptibility. This case-control study aims to investigate the T1D susceptibility association of alleles and genotypes of a widely investigated 14-bp insertion/deletion polymorphism in the
HLA-G
and to provide further evidence of the frequency distribution of class II
HLA-DR-DQ
-risk genotypes in T1D children and adolescents in the Brazilian population. The deletion allele and the homozygous deletion genotype are associated with susceptibility to T1D and the insertion allele and the heterozygous deletion/insertion genotype are associated with protection from T1D. We also confirm that genetic susceptibility to T1D is associated with the
DRB1*03:01-DQA1*05:01-DQB1*02:01
and
DRB1*04-DQA1*03:01-DQB1*03:02
haplotypes in Brazilian northeast region. The DR3-DQ2/DR4-DQ8 genotype conferred the highest detected risk for T1D. Our results identify a novel association of the 14-bp deletion allele and the homozygous deletion genotype with T1D development and provide additional evidence of the importance of
HLA
class II heterozygous DR3-DQ2/DR4-DQ8 genotype in T1D susceptibility.</description><identifier>ISSN: 1466-4879</identifier><identifier>EISSN: 1476-5470</identifier><identifier>DOI: 10.1038/gene.2015.45</identifier><identifier>PMID: 26492519</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>45/22 ; 45/29 ; 45/77 ; 631/208/727/2000 ; 631/250/249/1313/1418 ; Adaptive immunity ; Adolescent ; Alleles ; Biomedical and Life Sciences ; Biomedicine ; Brazil ; Cancer Research ; Case-Control Studies ; Child ; Development and progression ; Diabetes ; Diabetes mellitus (insulin dependent) ; Diabetes Mellitus, Type 1 - genetics ; Diabetes Mellitus, Type 1 - immunology ; Disease susceptibility ; DQA1 protein ; Drb1 protein ; Female ; Gene deletion ; Gene Expression ; Gene polymorphism ; Genetic aspects ; Genetic polymorphisms ; Genetic Predisposition to Disease ; Genetic research ; Genotype & phenotype ; Haplotypes ; Health aspects ; Histocompatibility antigen HLA ; Histocompatibility antigens ; HLA antigens ; HLA histocompatibility antigens ; HLA-D Antigens - genetics ; HLA-D Antigens - immunology ; HLA-G Antigens - genetics ; HLA-G Antigens - immunology ; Human Genetics ; Humans ; Immune response ; Immunological tolerance ; Immunology ; Immunomodulation ; Insertion ; Male ; original-article ; Polymorphism ; Polymorphism, Genetic ; Population genetics ; Risk factors ; Susceptibility ; Type 1 diabetes</subject><ispartof>Genes and immunity, 2016-01, Vol.17 (1), p.13-18</ispartof><rights>Macmillan Publishers Limited 2016</rights><rights>COPYRIGHT 2016 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Jan 2016</rights><rights>Macmillan Publishers Limited 2016.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c690t-146e8dfb693ac22393d212399f8d085d6b88b23de79eb24183681b8507e119783</citedby><cites>FETCH-LOGICAL-c690t-146e8dfb693ac22393d212399f8d085d6b88b23de79eb24183681b8507e119783</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/gene.2015.45$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/gene.2015.45$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51298</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26492519$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Silva, H P V</creatorcontrib><creatorcontrib>Ururahy, M A G</creatorcontrib><creatorcontrib>Souza, K S C</creatorcontrib><creatorcontrib>Loureiro, M B</creatorcontrib><creatorcontrib>Oliveira, Y M C</creatorcontrib><creatorcontrib>Oliveira, G H M</creatorcontrib><creatorcontrib>Luchessi, A D</creatorcontrib><creatorcontrib>Carvalho, K T C</creatorcontrib><creatorcontrib>Freitas, J C O C</creatorcontrib><creatorcontrib>Donadi, E A</creatorcontrib><creatorcontrib>Hirata, R D C</creatorcontrib><creatorcontrib>Almeida, M G</creatorcontrib><creatorcontrib>Arrais, R F</creatorcontrib><creatorcontrib>Hirata, M H</creatorcontrib><creatorcontrib>Rezende, A A</creatorcontrib><title>The association between the HLA-G 14-bp insertion/deletion polymorphism and type 1 diabetes</title><title>Genes and immunity</title><addtitle>Genes Immun</addtitle><addtitle>Genes Immun</addtitle><description>Type 1 diabetes (T1D) is a multifactorial disease that has a strong genetic component. The
HLA-G
is a nonclassical
HLA
class I locus that is associated with immunomodulatory functions, including downregulation of innate and adaptive immune responses and induction of immune tolerance. However, there is currently limited information about the involvement of
HLA-G
in T1D susceptibility. This case-control study aims to investigate the T1D susceptibility association of alleles and genotypes of a widely investigated 14-bp insertion/deletion polymorphism in the
HLA-G
and to provide further evidence of the frequency distribution of class II
HLA-DR-DQ
-risk genotypes in T1D children and adolescents in the Brazilian population. The deletion allele and the homozygous deletion genotype are associated with susceptibility to T1D and the insertion allele and the heterozygous deletion/insertion genotype are associated with protection from T1D. We also confirm that genetic susceptibility to T1D is associated with the
DRB1*03:01-DQA1*05:01-DQB1*02:01
and
DRB1*04-DQA1*03:01-DQB1*03:02
haplotypes in Brazilian northeast region. The DR3-DQ2/DR4-DQ8 genotype conferred the highest detected risk for T1D. Our results identify a novel association of the 14-bp deletion allele and the homozygous deletion genotype with T1D development and provide additional evidence of the importance of
HLA
class II heterozygous DR3-DQ2/DR4-DQ8 genotype in T1D susceptibility.</description><subject>45/22</subject><subject>45/29</subject><subject>45/77</subject><subject>631/208/727/2000</subject><subject>631/250/249/1313/1418</subject><subject>Adaptive immunity</subject><subject>Adolescent</subject><subject>Alleles</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brazil</subject><subject>Cancer Research</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Diabetes mellitus (insulin dependent)</subject><subject>Diabetes Mellitus, Type 1 - genetics</subject><subject>Diabetes Mellitus, Type 1 - immunology</subject><subject>Disease susceptibility</subject><subject>DQA1 protein</subject><subject>Drb1 protein</subject><subject>Female</subject><subject>Gene deletion</subject><subject>Gene Expression</subject><subject>Gene polymorphism</subject><subject>Genetic aspects</subject><subject>Genetic polymorphisms</subject><subject>Genetic Predisposition to Disease</subject><subject>Genetic research</subject><subject>Genotype & phenotype</subject><subject>Haplotypes</subject><subject>Health aspects</subject><subject>Histocompatibility antigen HLA</subject><subject>Histocompatibility antigens</subject><subject>HLA antigens</subject><subject>HLA histocompatibility antigens</subject><subject>HLA-D Antigens - genetics</subject><subject>HLA-D Antigens - immunology</subject><subject>HLA-G Antigens - genetics</subject><subject>HLA-G Antigens - immunology</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunological tolerance</subject><subject>Immunology</subject><subject>Immunomodulation</subject><subject>Insertion</subject><subject>Male</subject><subject>original-article</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Population genetics</subject><subject>Risk factors</subject><subject>Susceptibility</subject><subject>Type 1 diabetes</subject><issn>1466-4879</issn><issn>1476-5470</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqN0s9rFDEUB_BBFFurN88y4EXB2eZNfkxyXIq2hQVB68lDyEzebKfMJGMyS93_3oxbdVdKlRwSkk--CY-XZS-BLIBQebpGh4uSAF8w_ig7BlaJgrOKPJ7XQhRMVuooexbjDSEgQKin2VEpmCo5qOPs69U15iZG33Rm6rzLa5xuEV0-pf2L1bI4z4EV9Zh3LmKYxanFHn_S0ffbwYfxuotDbpzNp-2IOeS2MykF4_PsSWv6iC_u5pPsy4f3V2cXxerj-eXZclU0QpGpSL9EadtaKGqasqSK2hLSpFppieRW1FLWJbVYKaxLBpIKCbXkpEIAVUl6kr3Z5Y7Bf9tgnPTQxQb73jj0m6ihElxJ4FQk-voveuM3waXf6VQTqKjgRD2koOKSKyYY_aPWpkfdudZPwTTz03qZYogQoNSDirGSU84UT2pxj0rD4tA13mHbpf2D2P-6sP_C24MLyUz4fVqbTYz68vOnw_B_2f3cdzvbBB9jwFaPoRtM2Gogem5QPTeonhtUs5m_uivtph7Q_sa_OjKBYgdiOnJrDHu1vy_wB5C758A</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Silva, H P V</creator><creator>Ururahy, M A G</creator><creator>Souza, K S C</creator><creator>Loureiro, M B</creator><creator>Oliveira, Y M C</creator><creator>Oliveira, G H M</creator><creator>Luchessi, A D</creator><creator>Carvalho, K T C</creator><creator>Freitas, J C O C</creator><creator>Donadi, E A</creator><creator>Hirata, R D C</creator><creator>Almeida, M G</creator><creator>Arrais, R F</creator><creator>Hirata, M H</creator><creator>Rezende, A A</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>ISR</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope></search><sort><creationdate>20160101</creationdate><title>The association between the HLA-G 14-bp insertion/deletion polymorphism and type 1 diabetes</title><author>Silva, H P V ; Ururahy, M A G ; Souza, K S C ; Loureiro, M B ; Oliveira, Y M C ; Oliveira, G H M ; Luchessi, A D ; Carvalho, K T C ; Freitas, J C O C ; Donadi, E A ; Hirata, R D C ; Almeida, M G ; Arrais, R F ; Hirata, M H ; Rezende, A A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c690t-146e8dfb693ac22393d212399f8d085d6b88b23de79eb24183681b8507e119783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>45/22</topic><topic>45/29</topic><topic>45/77</topic><topic>631/208/727/2000</topic><topic>631/250/249/1313/1418</topic><topic>Adaptive immunity</topic><topic>Adolescent</topic><topic>Alleles</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brazil</topic><topic>Cancer Research</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Diabetes mellitus (insulin dependent)</topic><topic>Diabetes Mellitus, Type 1 - genetics</topic><topic>Diabetes Mellitus, Type 1 - immunology</topic><topic>Disease susceptibility</topic><topic>DQA1 protein</topic><topic>Drb1 protein</topic><topic>Female</topic><topic>Gene deletion</topic><topic>Gene Expression</topic><topic>Gene polymorphism</topic><topic>Genetic aspects</topic><topic>Genetic polymorphisms</topic><topic>Genetic Predisposition to Disease</topic><topic>Genetic research</topic><topic>Genotype & phenotype</topic><topic>Haplotypes</topic><topic>Health aspects</topic><topic>Histocompatibility antigen HLA</topic><topic>Histocompatibility antigens</topic><topic>HLA antigens</topic><topic>HLA histocompatibility antigens</topic><topic>HLA-D Antigens - genetics</topic><topic>HLA-D Antigens - immunology</topic><topic>HLA-G Antigens - genetics</topic><topic>HLA-G Antigens - immunology</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunological tolerance</topic><topic>Immunology</topic><topic>Immunomodulation</topic><topic>Insertion</topic><topic>Male</topic><topic>original-article</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Population genetics</topic><topic>Risk factors</topic><topic>Susceptibility</topic><topic>Type 1 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Silva, H P V</creatorcontrib><creatorcontrib>Ururahy, M A G</creatorcontrib><creatorcontrib>Souza, K S C</creatorcontrib><creatorcontrib>Loureiro, M B</creatorcontrib><creatorcontrib>Oliveira, Y M C</creatorcontrib><creatorcontrib>Oliveira, G H M</creatorcontrib><creatorcontrib>Luchessi, A D</creatorcontrib><creatorcontrib>Carvalho, K T C</creatorcontrib><creatorcontrib>Freitas, J C O C</creatorcontrib><creatorcontrib>Donadi, E A</creatorcontrib><creatorcontrib>Hirata, R D 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C</au><au>Freitas, J C O C</au><au>Donadi, E A</au><au>Hirata, R D C</au><au>Almeida, M G</au><au>Arrais, R F</au><au>Hirata, M H</au><au>Rezende, A A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The association between the HLA-G 14-bp insertion/deletion polymorphism and type 1 diabetes</atitle><jtitle>Genes and immunity</jtitle><stitle>Genes Immun</stitle><addtitle>Genes Immun</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>17</volume><issue>1</issue><spage>13</spage><epage>18</epage><pages>13-18</pages><issn>1466-4879</issn><eissn>1476-5470</eissn><abstract>Type 1 diabetes (T1D) is a multifactorial disease that has a strong genetic component. The
HLA-G
is a nonclassical
HLA
class I locus that is associated with immunomodulatory functions, including downregulation of innate and adaptive immune responses and induction of immune tolerance. However, there is currently limited information about the involvement of
HLA-G
in T1D susceptibility. This case-control study aims to investigate the T1D susceptibility association of alleles and genotypes of a widely investigated 14-bp insertion/deletion polymorphism in the
HLA-G
and to provide further evidence of the frequency distribution of class II
HLA-DR-DQ
-risk genotypes in T1D children and adolescents in the Brazilian population. The deletion allele and the homozygous deletion genotype are associated with susceptibility to T1D and the insertion allele and the heterozygous deletion/insertion genotype are associated with protection from T1D. We also confirm that genetic susceptibility to T1D is associated with the
DRB1*03:01-DQA1*05:01-DQB1*02:01
and
DRB1*04-DQA1*03:01-DQB1*03:02
haplotypes in Brazilian northeast region. The DR3-DQ2/DR4-DQ8 genotype conferred the highest detected risk for T1D. Our results identify a novel association of the 14-bp deletion allele and the homozygous deletion genotype with T1D development and provide additional evidence of the importance of
HLA
class II heterozygous DR3-DQ2/DR4-DQ8 genotype in T1D susceptibility.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26492519</pmid><doi>10.1038/gene.2015.45</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1466-4879 |
| ispartof | Genes and immunity, 2016-01, Vol.17 (1), p.13-18 |
| issn | 1466-4879 1476-5470 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1765981536 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | 45/22 45/29 45/77 631/208/727/2000 631/250/249/1313/1418 Adaptive immunity Adolescent Alleles Biomedical and Life Sciences Biomedicine Brazil Cancer Research Case-Control Studies Child Development and progression Diabetes Diabetes mellitus (insulin dependent) Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Disease susceptibility DQA1 protein Drb1 protein Female Gene deletion Gene Expression Gene polymorphism Genetic aspects Genetic polymorphisms Genetic Predisposition to Disease Genetic research Genotype & phenotype Haplotypes Health aspects Histocompatibility antigen HLA Histocompatibility antigens HLA antigens HLA histocompatibility antigens HLA-D Antigens - genetics HLA-D Antigens - immunology HLA-G Antigens - genetics HLA-G Antigens - immunology Human Genetics Humans Immune response Immunological tolerance Immunology Immunomodulation Insertion Male original-article Polymorphism Polymorphism, Genetic Population genetics Risk factors Susceptibility Type 1 diabetes |
| title | The association between the HLA-G 14-bp insertion/deletion polymorphism and type 1 diabetes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-22T05%3A20%3A20IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=The%20association%20between%20the%20HLA-G%2014-bp%20insertion/deletion%20polymorphism%20and%20type%201%20diabetes&rft.jtitle=Genes%20and%20immunity&rft.au=Silva,%20H%20P%20V&rft.date=2016-01-01&rft.volume=17&rft.issue=1&rft.spage=13&rft.epage=18&rft.pages=13-18&rft.issn=1466-4879&rft.eissn=1476-5470&rft_id=info:doi/10.1038/gene.2015.45&rft_dat=%3Cgale_proqu%3EA442535495%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1758594643&rft_id=info:pmid/26492519&rft_galeid=A442535495&rfr_iscdi=true |