HLA Class II Allele Analyses Implicate Common Genetic Components in Type 1 and Non–Insulin-Treated Type 2 Diabetes

Abstract Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density impute...

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Published inThe journal of clinical endocrinology and metabolism Vol. 105; no. 3; pp. e245 - e254
Main Authors Jacobi, Thomas, Massier, Lucas, Klöting, Nora, Horn, Katrin, Schuch, Alexander, Ahnert, Peter, Engel, Christoph, Löffler, Markus, Burkhardt, Ralph, Thiery, Joachim, Tönjes, Anke, Stumvoll, Michael, Blüher, Matthias, Doxiadis, Ilias, Scholz, Markus, Kovacs, Peter
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Published US Oxford University Press 01.03.2020
Copyright Oxford University Press
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Abstract Abstract Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes. Objectives and Design Three cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted. Results In a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non–insulin-treated diabetes (OR 1.37; P = 0.002). Conclusions Genetic variation in the HLA class II locus exerts risk and protective effects on non–insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.
AbstractList Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes. Objectives and Design Three cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted. Results In a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non–insulin-treated diabetes (OR 1.37; P = 0.002). Conclusions Genetic variation in the HLA class II locus exerts risk and protective effects on non–insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.
Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes. Three cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted. In a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non-insulin-treated diabetes (OR 1.37; P = 0.002). Genetic variation in the HLA class II locus exerts risk and protective effects on non-insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.
Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes.CONTEXTCommon genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes.Three cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted.OBJECTIVES AND DESIGNThree cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted.In a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non-insulin-treated diabetes (OR 1.37; P = 0.002).RESULTSIn a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non-insulin-treated diabetes (OR 1.37; P = 0.002).Genetic variation in the HLA class II locus exerts risk and protective effects on non-insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.CONCLUSIONSGenetic variation in the HLA class II locus exerts risk and protective effects on non-insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.
Abstract Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II genes in the pathophysiology of type 1 diabetes, the aim of the present study was to test the association of high density imputed human leukocyte antigen (HLA) genotypes with type 2 diabetes. Objectives and Design Three cohorts (Ntotal = 10 413) from Leipzig, Germany were included in this study: LIFE-Adult (N = 4649), LIFE-Heart (N = 4815) and the Sorbs (N = 949) cohort. Detailed metabolic phenotyping and genome-wide single nucleotide polymorphism (SNP) data were available for all subjects. Using 1000 Genome imputation data, HLA genotypes were imputed on 4-digit level and association tests for type 2 diabetes, and related metabolic traits were conducted. Results In a meta-analysis including all 3 cohorts, the absence of HLA-DRB5 was associated with increased risk of type 2 diabetes (P = 0.001). In contrast, HLA-DQB*06:02 and HLA-DQA*01:02 had a protective effect on type 2 diabetes (P = 0.005 and 0.003, respectively). Both alleles are part of the well-established type 1 diabetes protective haplotype DRB1*15:01~DQA1*01:02~DQB1*06:02, which was also associated with reduced risk of type 2 diabetes (OR 0.84; P = 0.005). On the contrary, the DRB1*07:01~DQA1*02:01~DQB1*03:03 was identified as a risk haplotype in non–insulin-treated diabetes (OR 1.37; P = 0.002). Conclusions Genetic variation in the HLA class II locus exerts risk and protective effects on non–insulin-treated type 2 diabetes. Our data suggest that the genetic architecture of type 1 diabetes and type 2 diabetes might share common components on the HLA class II locus.
Author Schuch, Alexander
Thiery, Joachim
Engel, Christoph
Scholz, Markus
Massier, Lucas
Tönjes, Anke
Ahnert, Peter
Jacobi, Thomas
Blüher, Matthias
Horn, Katrin
Kovacs, Peter
Löffler, Markus
Doxiadis, Ilias
Klöting, Nora
Burkhardt, Ralph
Stumvoll, Michael
AuthorAffiliation University of Leipzig Medical Center, IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Leipzig, Germany LIFE Research Centre for Civilization Diseases, University of Leipzig, Leipzig, Germany Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Regensburg, Regensburg, Germany Institute of Laboratory Medicine and Clinical Chemistry, University of Leipzig, Leipzig, Germany Medical Department III – Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Germany Institute for Transfusion Medicine, University Hospital of Leipzig, Leipzig, Germany
AuthorAffiliation_xml – name: University of Leipzig Medical Center, IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany Institute for Medical Informatics, Statistics and Epidemiology, University of Leipzig, Leipzig, Germany LIFE Research Centre for Civilization Diseases, University of Leipzig, Leipzig, Germany Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Regensburg, Regensburg, Germany Institute of Laboratory Medicine and Clinical Chemistry, University of Leipzig, Leipzig, Germany Medical Department III – Endocrinology, Nephrology, Rheumatology, University of Leipzig Medical Center, Germany Institute for Transfusion Medicine, University Hospital of Leipzig, Leipzig, Germany
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  surname: Kovacs
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/31974565$$D View this record in MEDLINE/PubMed
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Cites_doi 10.1371/journal.pcbi.1002877
10.1186/1471-2156-12-67
10.1111/j.1744-313X.2006.00581.x
10.1155/2013/452537
10.1086/282771
10.1002/jmri.26754
10.1097/MD.0000000000003858
10.1084/jem.179.1.279
10.2337/db07-1331
10.1016/j.cmet.2013.02.009
10.2337/db16-1253
10.1093/nar/gku1166
10.1038/srep35005
10.2337/db15-1115
10.1007/BF00399956
10.2337/db18-0501
10.1007/s00125-016-4139-5
10.4049/jimmunol.160.7.3363
10.3389/fimmu.2017.00984
10.2337/diacare.24.4.796
10.2337/dc18-S002
10.1093/hmg/ddp423
10.2337/diabetes.48.1.150
10.1373/clinchem.2010.148270
10.2337/db13-1153
10.1111/cei.12687
10.1038/tpj.2013.18
10.4049/jimmunol.159.2.703
10.1371/journal.pone.0172444
10.7717/peerj.281
10.1038/ng1885
10.3324/haematol.2017.179119
10.1007/s00125-011-2122-8
10.2337/diabetes.48.5.983
10.1371/journal.pone.0029070
10.1111/j.1745-7599.2009.00399.x
10.1038/ng.3943
10.1186/s12889-015-1983-z
10.1371/journal.pgen.1005510
10.1016/S0198-8859(99)00146-9
10.1111/j.1463-1326.2008.00950.x
10.1007/s00125-006-0513-z
10.1007/s001250051202
10.1016/0197-2456(86)90046-2
10.1210/jc.2003-032084
10.1016/j.celrep.2014.09.004
10.2337/diabetes.54.suppl_2.S40
10.1007/s00251-011-0513-0
10.1016/S2213-8587(18)30051-2
10.1136/bmj.307.6897.155
10.1002/sim.1186
10.1016/j.humimm.2015.12.006
10.1007/s00125-003-1070-3
10.1007/BF00280883
10.2337/dc08-s243
10.4049/jimmunol.153.4.1665
10.1089/152091504774198124
10.4049/jimmunol.160.5.2365
10.1038/ejhg.2009.107
10.1016/j.clim.2005.08.017
10.1093/bioinformatics/bty633
10.1007/BF00401370
ContentType Journal Article
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Endocrine Society 2020. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
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IsPeerReviewed true
IsScholarly true
Issue 3
Keywords type 1 diabetes
haplotype
type 2 diabetes
single nucleotide polymorphism
genotype imputation
HLA class II
association
Language English
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References Stumvoll (2021122102015822900_CIT0032) 2001; 24
Karnes (2021122102015822900_CIT0016) 2017; 12
Raddrizzani (2021122102015822900_CIT0062) 1997; 159
Loeffler (2021122102015822900_CIT0017) 2015; 15
Nomura (2021122102015822900_CIT0041) 2006; 33
de Bakker (2021122102015822900_CIT0015) 2006; 38
R Core Team (2021122102015822900_CIT0025) 2018
Sanjeevi (2021122102015822900_CIT0038) 2000; 61
Nei (2021122102015822900_CIT0027) 1972; 106
Donath (2021122102015822900_CIT0049) 2008; 31 Suppl 2
Astill (2021122102015822900_CIT0055) 2003; 46
Lambert (2021122102015822900_CIT0003) 2004; 89
González-Galarza (2021122102015822900_CIT0026) 2015; 43
Tuomi (2021122102015822900_CIT0053) 1999; 48
van Lummel (2021122102015822900_CIT0066) 2019; 68
Brooks-Worrell (2021122102015822900_CIT0043) 1999; 48
Böni-Schnetzler (2021122102015822900_CIT0048) 2008; 10
Williams (2021122102015822900_CIT0013) 2011; 54
Beutner (2021122102015822900_CIT0018) 2011; 6
Gross (2021122102015822900_CIT0023) 2011; 12
Hrdinová (2021122102015822900_CIT0057) 2018; 103
Guo (2021122102015822900_CIT0011) 2016; 6
Horton (2021122102015822900_CIT0010) 1999; 42
Paradis (2021122102015822900_CIT0029) 2019; 35
Schwarzer (2021122102015822900_CIT0034) 2007; 7
Zavala (2021122102015822900_CIT0044) 1992; 35
Tönjes (2021122102015822900_CIT0021) 2010; 18
Cho (2021122102015822900_CIT0005) 2014; 9
Pfützner (2021122102015822900_CIT0065) 2004; 6
Ma (2021122102015822900_CIT0040) 2013; 2013
Tönjes (2021122102015822900_CIT0020) 2009; 18
DerSimonian (2021122102015822900_CIT0035) 1986; 7
Roark (2021122102015822900_CIT0039) 2014; 63
Rich (2021122102015822900_CIT0008) 1993; 36
Wucherpfennig (2021122102015822900_CIT0061) 1994; 179
Ahlqvist (2021122102015822900_CIT0006) 2018; 6
Erlich (2021122102015822900_CIT0054) 2008; 57
Barbosa (2021122102015822900_CIT0058) 2006; 118
Pappas (2021122102015822900_CIT0037) 2016; 77
de Vries (2021122102015822900_CIT0056) 2017; 60
Massier (2021122102015822900_CIT0050)
Southwood (2021122102015822900_CIT0059) 1998; 160
American Diabetes Association 2 (2021122102015822900_CIT0022) 2018; 41
Zhao (2021122102015822900_CIT0014) 2017; 49
Viechtbauer (2021122102015822900_CIT0033) 2010
Chen (2021122102015822900_CIT0046) 2019; 50
Vogt (2021122102015822900_CIT0060) 1994; 153
Tuomilehto-Wolf (2021122102015822900_CIT0009) 1993; 307
Matthews (2021122102015822900_CIT0031) 1985; 28
Tuomi (2021122102015822900_CIT0007) 2005; 54 Suppl 2
Desai (2021122102015822900_CIT0002) 2007; 50
Deng (2021122102015822900_CIT0004) 2013; 17
Zheng (2021122102015822900_CIT0030) 2014; 14
Gibson (2021122102015822900_CIT0064) 2015; 182
Scott (2021122102015822900_CIT0012) 2017; 66
Zhao (2021122102015822900_CIT0051) 2016; 65
Appel (2021122102015822900_CIT0042) 2009; 21
Brooks-Worrell (2021122102015822900_CIT0045) 2011; 57
Ettinger (2021122102015822900_CIT0063) 1998; 160
Greenbaum (2021122102015822900_CIT0001) 2011; 63
Dilthey (2021122102015822900_CIT0024) 2013; 9
Burkhardt (2021122102015822900_CIT0019) 2015; 11
Higgins (2021122102015822900_CIT0036) 2002; 21
Scholz (2021122102015822900_CIT0052) 2017; 8
Kamvar (2021122102015822900_CIT0028) 2014; 2
Dong (2021122102015822900_CIT0047) 2016; 95
References_xml – volume: 9
  start-page: e1002877
  issue: 2
  year: 2013
  ident: 2021122102015822900_CIT0024
  article-title: Multi-population classical HLA type imputation
  publication-title: Plos Comput Biol.
  doi: 10.1371/journal.pcbi.1002877
– volume: 12
  start-page: 67
  year: 2011
  ident: 2021122102015822900_CIT0023
  article-title: Population-genetic comparison of the Sorbian isolate population in Germany with the German KORA population using genome-wide SNP arrays
  publication-title: BMC Genet.
  doi: 10.1186/1471-2156-12-67
– volume: 33
  start-page: 117
  issue: 2
  year: 2006
  ident: 2021122102015822900_CIT0041
  article-title: Genetic analysis of HLA, NA and HPA typing in type 2 diabetes and ASO
  publication-title: Int J Immunogenet.
  doi: 10.1111/j.1744-313X.2006.00581.x
– volume: 2013
  start-page: 452537
  year: 2013
  ident: 2021122102015822900_CIT0040
  article-title: Association of the HLA-DQA1 and HLA-DQB1 alleles in type 2 diabetes mellitus and diabetic nephropathy in the han ethnicity of China
  publication-title: J Diabetes Res.
  doi: 10.1155/2013/452537
– volume: 106
  start-page: 283
  year: 1972
  ident: 2021122102015822900_CIT0027
  article-title: Genetic distance between populations
  publication-title: The American Naturalist
  doi: 10.1086/282771
– volume: 50
  start-page: 1905
  issue: 6
  year: 2019
  ident: 2021122102015822900_CIT0046
  article-title: Magnetic resonance imaging: proton density fat fraction for assessment of pancreatic fatty infiltration during progression of T2DM bama minipigs
  publication-title: J Magn Reson Imaging
  doi: 10.1002/jmri.26754
– volume: 95
  issue: 23
  year: 2016
  ident: 2021122102015822900_CIT0047
  article-title: Noninvasive fat quantification of the liver and pancreas may provide potential biomarkers of impaired glucose tolerance and type 2 diabetes
  publication-title: Medicine (Baltimore)
  doi: 10.1097/MD.0000000000003858
– volume: 179
  start-page: 279
  year: 1994
  ident: 2021122102015822900_CIT0061
  article-title: Structural requirements for binding of an immunodominant myelin basic protein peptide to DR2 isotypes and for its recognition by human T cell clones
  publication-title: Journal of Experimental Medicine
  doi: 10.1084/jem.179.1.279
– volume: 57
  start-page: 1084
  issue: 4
  year: 2008
  ident: 2021122102015822900_CIT0054
  article-title: HLA DR-DQ haplotypes and genotypes and type 1 diabetes risk: analysis of the type 1 diabetes genetics consortium families
  publication-title: Diabetes.
  doi: 10.2337/db07-1331
– volume: 17
  start-page: 411
  issue: 3
  year: 2013
  ident: 2021122102015822900_CIT0004
  article-title: Class II major histocompatibility complex plays an essential role in obesity-induced adipose inflammation
  publication-title: Cell Metab.
  doi: 10.1016/j.cmet.2013.02.009
– volume: 66
  start-page: 2888
  issue: 11
  year: 2017
  ident: 2021122102015822900_CIT0012
  article-title: An expanded genome-wide association study of type 2 diabetes in Europeans
  publication-title: Diabetes.
  doi: 10.2337/db16-1253
– volume: 43
  start-page: D784
  issue: Database issue
  year: 2015
  ident: 2021122102015822900_CIT0026
  article-title: Allele frequency net 2015 update: new features for HLA epitopes, KIR and disease and HLA adverse drug reaction associations
  publication-title: Nucleic Acids Res.
  doi: 10.1093/nar/gku1166
– volume: 6
  start-page: 35005
  year: 2016
  ident: 2021122102015822900_CIT0011
  article-title: The relationships between HLA class II alleles and antigens with gestational diabetes mellitus: a meta-analysis
  publication-title: Sci Rep.
  doi: 10.1038/srep35005
– volume: 65
  start-page: 710
  issue: 3
  year: 2016
  ident: 2021122102015822900_CIT0051
  article-title: Next-generation sequencing reveals that HLA-DRB3, -DRB4, and -DRB5 may be associated with islet autoantibodies and risk for childhood type 1 diabetes
  publication-title: Diabetes.
  doi: 10.2337/db15-1115
– volume: 36
  start-page: 234
  issue: 3
  year: 1993
  ident: 2021122102015822900_CIT0008
  article-title: HLA-associated susceptibility to type 2 (non-insulin-dependent) diabetes mellitus: the Wadena City Health Study
  publication-title: Diabetologia.
  doi: 10.1007/BF00399956
– volume: 68
  start-page: 787
  issue: 4
  year: 2019
  ident: 2021122102015822900_CIT0066
  article-title: Epitope stealing as a mechanism of dominant protection by HLA-DQ6 in type 1 diabetes
  publication-title: Diabetes.
  doi: 10.2337/db18-0501
– volume: 60
  start-page: 280
  year: 2017
  ident: 2021122102015822900_CIT0056
  article-title: ADAMTS13 activity as a novel risk factor for incident type 2 diabetes mellitus: a population-based cohort study
  publication-title: Diabetologia
  doi: 10.1007/s00125-016-4139-5
– volume: 160
  start-page: 3363
  year: 1998
  ident: 2021122102015822900_CIT0059
  article-title: Several common HLA-DR types share largely overlapping peptide binding repertoires
  publication-title: The Journal of Immunology
  doi: 10.4049/jimmunol.160.7.3363
– volume: 8
  start-page: 984
  year: 2017
  ident: 2021122102015822900_CIT0052
  article-title: Human leukocyte antigen (HLA)-DRB1*15:01 and HLA-DRB5*01:01 present complementary peptide repertoires
  publication-title: Front Immunol.
  doi: 10.3389/fimmu.2017.00984
– volume: 24
  start-page: 796
  issue: 4
  year: 2001
  ident: 2021122102015822900_CIT0032
  article-title: Oral glucose tolerance test indexes for insulin sensitivity and secretion based on various availabilities of sampling times
  publication-title: Diabetes Care.
  doi: 10.2337/diacare.24.4.796
– volume: 41
  start-page: S13
  year: 2018
  ident: 2021122102015822900_CIT0022
  article-title: Classification and diagnosis of diabetes: standards of medical care in diabetes—2018
  publication-title: Diabetes Care
  doi: 10.2337/dc18-S002
– volume: 18
  start-page: 4662
  issue: 23
  year: 2009
  ident: 2021122102015822900_CIT0020
  article-title: Genetic variation in GPR133 is associated with height: genome wide association study in the self-contained population of Sorbs
  publication-title: Hum Mol Genet.
  doi: 10.1093/hmg/ddp423
– volume: 48
  start-page: 150
  issue: 1
  year: 1999
  ident: 2021122102015822900_CIT0053
  article-title: Clinical and genetic characteristics of type 2 diabetes with and without GAD antibodies
  publication-title: Diabetes.
  doi: 10.2337/diabetes.48.1.150
– volume: 57
  start-page: 158
  issue: 2
  year: 2011
  ident: 2021122102015822900_CIT0045
  article-title: Is diabetes mellitus a continuous spectrum?
  publication-title: Clin Chem.
  doi: 10.1373/clinchem.2010.148270
– volume: 63
  start-page: 323
  issue: 1
  year: 2014
  ident: 2021122102015822900_CIT0039
  article-title: Multiple HLA epitopes contribute to type 1 diabetes susceptibility
  publication-title: Diabetes.
  doi: 10.2337/db13-1153
– volume: 182
  start-page: 251
  issue: 3
  year: 2015
  ident: 2021122102015822900_CIT0064
  article-title: Proinsulin multi-peptide immunotherapy induces antigen-specific regulatory T cells and limits autoimmunity in a humanized model
  publication-title: Clin Exp Immunol.
  doi: 10.1111/cei.12687
– volume: 14
  start-page: 192
  issue: 2
  year: 2014
  ident: 2021122102015822900_CIT0030
  article-title: HIBAG–HLA genotype imputation with attribute bagging
  publication-title: Pharmacogenomics J.
  doi: 10.1038/tpj.2013.18
– volume: 159
  start-page: 703
  year: 1997
  ident: 2021122102015822900_CIT0062
  article-title: Different modes of peptide interaction enable HLA-DQ and HLA-DR molecules to bind diverse peptide repertoires
  publication-title: The Journal of Immunology
  doi: 10.4049/jimmunol.159.2.703
– volume: 12
  start-page: e0172444
  issue: 2
  year: 2017
  ident: 2021122102015822900_CIT0016
  article-title: Comparison of HLA allelic imputation programs
  publication-title: Plos One.
  doi: 10.1371/journal.pone.0172444
– volume: 2
  start-page: e281
  year: 2014
  ident: 2021122102015822900_CIT0028
  article-title: Poppr: an R package for genetic analysis of populations with clonal, partially clonal, and/or sexual reproduction
  publication-title: Peerj.
  doi: 10.7717/peerj.281
– volume: 38
  start-page: 1166
  issue: 10
  year: 2006
  ident: 2021122102015822900_CIT0015
  article-title: A high-resolution HLA and SNP haplotype map for disease association studies in the extended human MHC
  publication-title: Nat Genet.
  doi: 10.1038/ng1885
– volume: 103
  start-page: 1083
  issue: 6
  year: 2018
  ident: 2021122102015822900_CIT0057
  article-title: Mass spectrometry-assisted identification of ADAMTS13-derived peptides presented on HLA-DR and HLA-DQ
  publication-title: Haematologica.
  doi: 10.3324/haematol.2017.179119
– volume: 54
  start-page: 1684
  issue: 7
  year: 2011
  ident: 2021122102015822900_CIT0013
  article-title: HLA-DRB1 reduces the risk of type 2 diabetes mellitus by increased insulin secretion
  publication-title: Diabetologia.
  doi: 10.1007/s00125-011-2122-8
– volume: 48
  start-page: 983
  issue: 5
  year: 1999
  ident: 2021122102015822900_CIT0043
  article-title: Cellular immune responses to human islet proteins in antibody- positive type 2 diabetic patients
  publication-title: Diabetes.
  doi: 10.2337/diabetes.48.5.983
– volume-title: R: A Language and Environment for Statistical Computing
  year: 2018
  ident: 2021122102015822900_CIT0025
– volume: 6
  start-page: e29070
  issue: 12
  year: 2011
  ident: 2021122102015822900_CIT0018
  article-title: Rationale and design of the Leipzig (LIFE) Heart Study: phenotyping and cardiovascular characteristics of patients with coronary artery disease
  publication-title: Plos One.
  doi: 10.1371/journal.pone.0029070
– volume: 21
  start-page: 156
  issue: 3
  year: 2009
  ident: 2021122102015822900_CIT0042
  article-title: Latent autoimmune diabetes of adulthood (LADA): an often misdiagnosed type of diabetes mellitus
  publication-title: J Am Acad Nurse Pract.
  doi: 10.1111/j.1745-7599.2009.00399.x
– year: 2010
  ident: 2021122102015822900_CIT0033
  article-title: Conducting meta-analyses in R with the metafor package
– volume: 49
  start-page: 1450
  issue: 10
  year: 2017
  ident: 2021122102015822900_CIT0014
  article-title: Identification of new susceptibility loci for type 2 diabetes and shared etiological pathways with coronary heart disease
  publication-title: Nat Genet.
  doi: 10.1038/ng.3943
– volume: 15
  start-page: 691
  year: 2015
  ident: 2021122102015822900_CIT0017
  article-title: The LIFE-Adult-Study: objectives and design of a population-based cohort study with 10 000 deeply phenotyped adults in Germany
  publication-title: BMC Public Health.
  doi: 10.1186/s12889-015-1983-z
– volume: 11
  start-page: e1005510
  issue: 9
  year: 2015
  ident: 2021122102015822900_CIT0019
  article-title: Integration of genome-wide SNP data and gene-expression profiles reveals six novel loci and regulatory mechanisms for amino acids and acylcarnitines in whole blood
  publication-title: Plos Genet.
  doi: 10.1371/journal.pgen.1005510
– volume: 61
  start-page: 148
  issue: 2
  year: 2000
  ident: 2021122102015822900_CIT0038
  article-title: HLA-DQ6-mediated protection in IDDM
  publication-title: Hum Immunol.
  doi: 10.1016/S0198-8859(99)00146-9
– volume: 10
  start-page: 201
  year: 2008
  ident: 2021122102015822900_CIT0048
  article-title: Insulitis in type 2 diabetes
  publication-title: Diabetes, Obesity and Metabolism
  doi: 10.1111/j.1463-1326.2008.00950.x
– volume: 50
  start-page: 68
  issue: 1
  year: 2007
  ident: 2021122102015822900_CIT0002
  article-title: An association analysis of the HLA gene region in latent autoimmune diabetes in adults
  publication-title: Diabetologia.
  doi: 10.1007/s00125-006-0513-z
– volume: 42
  start-page: 608
  issue: 5
  year: 1999
  ident: 2021122102015822900_CIT0010
  article-title: Genetic heterogeneity of autoimmune diabetes: age of presentation in adults is influenced by HLA DRB1 and DQB1 genotypes (UKPDS 43). UK Prospective Diabetes Study (UKPDS) Group
  publication-title: Diabetologia.
  doi: 10.1007/s001250051202
– volume: 7
  start-page: 177
  issue: 3
  year: 1986
  ident: 2021122102015822900_CIT0035
  article-title: Meta-analysis in clinical trials
  publication-title: Control Clin Trials.
  doi: 10.1016/0197-2456(86)90046-2
– volume: 89
  start-page: 4037
  issue: 8
  year: 2004
  ident: 2021122102015822900_CIT0003
  article-title: Absolute risk of childhood-onset type 1 diabetes defined by human leukocyte antigen class II genotype: a population-based study in the United Kingdom
  publication-title: J Clin Endocrinol Metab.
  doi: 10.1210/jc.2003-032084
– volume: 9
  start-page: 605
  issue: 2
  year: 2014
  ident: 2021122102015822900_CIT0005
  article-title: An MHC II-dependent activation loop between adipose tissue macrophages and CD4+ T cells controls obesity-induced inflammation
  publication-title: Cell Rep.
  doi: 10.1016/j.celrep.2014.09.004
– volume: 54 Suppl 2
  start-page: S40
  year: 2005
  ident: 2021122102015822900_CIT0007
  article-title: Type 1 and type 2 diabetes: what do they have in common?
  publication-title: Diabetes.
  doi: 10.2337/diabetes.54.suppl_2.S40
– volume: 7
  start-page: 40
  year: 2007
  ident: 2021122102015822900_CIT0034
  article-title: meta: an R package for meta-analysis
  publication-title: R News
– volume: 63
  start-page: 325
  issue: 6
  year: 2011
  ident: 2021122102015822900_CIT0001
  article-title: Functional classification of class II human leukocyte antigen (HLA) molecules reveals seven different supertypes and a surprising degree of repertoire sharing across supertypes
  publication-title: Immunogenetics.
  doi: 10.1007/s00251-011-0513-0
– volume: 6
  start-page: 361
  issue: 5
  year: 2018
  ident: 2021122102015822900_CIT0006
  article-title: Novel subgroups of adult-onset diabetes and their association with outcomes: a data-driven cluster analysis of six variables
  publication-title: Lancet Diabetes Endocrinol.
  doi: 10.1016/S2213-8587(18)30051-2
– volume: 307
  start-page: 155
  issue: 6897
  year: 1993
  ident: 2021122102015822900_CIT0009
  article-title: Genetic susceptibility to non-insulin dependent diabetes mellitus and glucose intolerance are located in HLA region
  publication-title: Bmj.
  doi: 10.1136/bmj.307.6897.155
– volume: 21
  start-page: 1539
  issue: 11
  year: 2002
  ident: 2021122102015822900_CIT0036
  article-title: Quantifying heterogeneity in a meta-analysis
  publication-title: Stat Med.
  doi: 10.1002/sim.1186
– volume: 77
  start-page: 283
  issue: 3
  year: 2016
  ident: 2021122102015822900_CIT0037
  article-title: Bridging immunogenomic data analysis workflow gaps (BIGDAWG): an integrated case-control analysis pipeline
  publication-title: Hum Immunol.
  doi: 10.1016/j.humimm.2015.12.006
– volume: 46
  start-page: 496
  issue: 4
  year: 2003
  ident: 2021122102015822900_CIT0055
  article-title: Promiscuous binding of proinsulin peptides to Type 1 diabetes-permissive and -protective HLA class II molecules
  publication-title: Diabetologia.
  doi: 10.1007/s00125-003-1070-3
– volume: 28
  start-page: 412
  issue: 7
  year: 1985
  ident: 2021122102015822900_CIT0031
  article-title: Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man
  publication-title: Diabetologia.
  doi: 10.1007/BF00280883
– volume: 31 Suppl 2
  start-page: S161
  year: 2008
  ident: 2021122102015822900_CIT0049
  article-title: Islet inflammation in type 2 diabetes: from metabolic stress to therapy
  publication-title: Diabetes Care.
  doi: 10.2337/dc08-s243
– volume: 153
  start-page: 1665
  year: 1994
  ident: 2021122102015822900_CIT0060
  article-title: Ligand motifs of HLA-DRB5*0101 and DRB1*1501 molecules delineated from self-peptides
  publication-title: The Journal of Immunology
  doi: 10.4049/jimmunol.153.4.1665
– volume: 6
  start-page: 405
  issue: 3
  year: 2004
  ident: 2021122102015822900_CIT0065
  article-title: Role of intact proinsulin in diagnosis and treatment of type 2 diabetes mellitus
  publication-title: Diabetes Technol Ther.
  doi: 10.1089/152091504774198124
– volume: 160
  start-page: 2365
  year: 1998
  ident: 2021122102015822900_CIT0063
  article-title: A peptide binding Motif for HLA-DQA1*0102/DQB1*0602, the class II MHC molecule associated with dominant protection in insulin-dependent diabetes mellitus
  publication-title: The Journal of Immunology
  doi: 10.4049/jimmunol.160.5.2365
– volume: 18
  start-page: 104
  issue: 1
  year: 2010
  ident: 2021122102015822900_CIT0021
  article-title: Association of FTO variants with BMI and fat mass in the self-contained population of Sorbs in Germany
  publication-title: Eur J Hum Genet.
  doi: 10.1038/ejhg.2009.107
– volume: 118
  start-page: 42
  issue: 1
  year: 2006
  ident: 2021122102015822900_CIT0058
  article-title: Clinical link between MHC class II haplotype and interferon-beta (IFN-beta) immunogenicity
  publication-title: Clin Immunol.
  doi: 10.1016/j.clim.2005.08.017
– volume: 35
  start-page: 526
  issue: 3
  year: 2019
  ident: 2021122102015822900_CIT0029
  article-title: ape 5.0: an environment for modern phylogenetics and evolutionary analyses in R
  publication-title: Bioinformatics.
  doi: 10.1093/bioinformatics/bty633
– ident: 2021122102015822900_CIT0050
  article-title: Data from: HLA Class II allele analyses implicate common genetic components in type 1 and non–insulin-treated type 2 diabetes.
– volume: 35
  start-page: 1159
  issue: 12
  year: 1992
  ident: 2021122102015822900_CIT0044
  article-title: Cellular and humoural autoimmunity markers in type 2 (non-insulin-dependent) diabetic patients with secondary drug failure
  publication-title: Diabetologia.
  doi: 10.1007/BF00401370
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Snippet Abstract Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of...
Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class II...
Context Common genetic susceptibility may underlie the frequently observed co-occurrence of type 1 and type 2 diabetes in families. Given the role of HLA class...
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SubjectTerms Alleles
Diabetes
Diabetes mellitus (insulin dependent)
Diabetes mellitus (non-insulin dependent)
DQA1 protein
Drb1 protein
Gene polymorphism
Genetic analysis
Genetic diversity
Genomes
Haplotypes
Histocompatibility antigen HLA
Insulin
Metabolism
Phenotyping
Single-nucleotide polymorphism
Title HLA Class II Allele Analyses Implicate Common Genetic Components in Type 1 and Non–Insulin-Treated Type 2 Diabetes
URI https://www.ncbi.nlm.nih.gov/pubmed/31974565
https://www.proquest.com/docview/2431027500
https://www.proquest.com/docview/2344274637
Volume 105
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