Next-Generation Sequencing Reveals That HLA-DRB3 , -DRB4 , and -DRB5 May Be Associated With Islet Autoantibodies and Risk for Childhood Type 1 Diabetes
The possible contribution of HLA-DRB3, -DRB4, and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 against either of the three amino acid variants R, W, or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respective...
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| Published in | Diabetes (New York, N.Y.) Vol. 65; no. 3; pp. 710 - 718 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Diabetes Association
01.03.2016
|
| Subjects | |
| Online Access | Get full text |
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| Abstract | The possible contribution of HLA-DRB3, -DRB4, and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 against either of the three amino acid variants R, W, or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respectively) at clinical diagnosis is unclear. Next-generation sequencing (NGS) was used to determine all DRB alleles in consecutively diagnosed patients ages 1–18 years with islet autoantibody–positive type 1 diabetes (n = 970) and control subjects (n = 448). DRB3, DRB4, or DRB5 alleles were tested for an association with the risk of DRB1 for autoantibodies, type 1 diabetes, or both. The association between type 1 diabetes and DRB1*03:01:01 was affected by DRB3*01:01:02 and DRB3*02:02:01. These DRB3 alleles were associated positively with GADA but negatively with ZnT8WA, IA-2A, and IAA. The negative association between type 1 diabetes and DRB1*13:01:01 was affected by DRB3*01:01:02 to increase the risk and by DRB3*02:02:01 to maintain a negative association. DRB4*01:03:01 was strongly associated with type 1 diabetes (P = 10−36), yet its association was extensively affected by DRB1 alleles from protective (DRB1*04:03:01) to high (DRB1*04:01:01) risk, but its association with DRB1*04:05:01 decreased the risk. HLA-DRB3, -DRB4, and -DRB5 affect type 1 diabetes risk and islet autoantibodies. HLA typing with NGS should prove useful to select participants for prevention or intervention trials. |
|---|---|
| AbstractList | The possible contribution of
HLA-DRB3
,
-DRB4
, and
-DRB5
alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 against either of the three amino acid variants R, W, or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respectively) at clinical diagnosis is unclear. Next-generation sequencing (NGS) was used to determine all
DRB
alleles in consecutively diagnosed patients ages 1–18 years with islet autoantibody–positive type 1 diabetes (
n
= 970) and control subjects (
n
= 448).
DRB3
,
DRB4
, or
DRB5
alleles were tested for an association with the risk of
DRB1
for autoantibodies, type 1 diabetes, or both. The association between type 1 diabetes and
DRB1
*03:01:01 was affected by
DRB3
*01:01:02 and
DRB3
*02:02:01. These
DRB3
alleles were associated positively with GADA but negatively with ZnT8WA, IA-2A, and IAA. The negative association between type 1 diabetes and
DRB1
*13:01:01 was affected by
DRB3
*01:01:02 to increase the risk and by
DRB3
*02:02:01 to maintain a negative association.
DRB4
*01:03:01 was strongly associated with type 1 diabetes (
P
= 10
−36
), yet its association was extensively affected by
DRB1
alleles from protective (
DRB1
*04:03:01) to high (
DRB1
*04:01:01) risk, but its association with
DRB1
*04:05:01 decreased the risk.
HLA-DRB3
,
-DRB4
, and
-DRB5
affect type 1 diabetes risk and islet autoantibodies.
HLA
typing with NGS should prove useful to select participants for prevention or intervention trials. The possible contribution of HLA-DRB3, -DRB4 and -DRB5 alleles to type 1 diabetes risk and to autoantibodies against insulin (IAA), GAD65 (GADA), IA-2 (IA-2A) or ZnT8 against either of the three amino acid variants, R, W or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respectively) at clinical diagnosis is unclear. Next generation sequencing (NGS) was therefore used to determine all DRB alleles in consecutively diagnosed, islet autoantibody positive 1-18 years old type 1 diabetes patients (n=970) and controls (n=448). It was tested whether DRB3, DRB4 or DRB5 alleles were associated with the risk of DRB1 for autoantibodies, type 1 diabetes, or both. The association between type 1 diabetes and DRB1*03:01:01 was affected by DRB3*01:01:02 and DRB3*02:02:01. These DRB3 alleles were associated positively with GADA but negatively with ZnT8WA, IA-2A and IAA. The negative association between type 1 diabetes and DRB1*13:01:01 was affected by DRB3*01:01:02 to increase the risk and by DRB3*02:02:01 to maintain a negative association. DRB4*01:03:01 was strongly associated with type 1 diabetes (p=10(-36)) yet its association was extensively affected by DRB1 alleles from protective (DRB1*04:03:01) to high (DRB1*04:01:01) risk but with DRB1:04:05:01 it decreased the risk. HLA-DRB3, -DRB4, and -DRB5 affect type 1 diabetes risk and islet autoantibodies. HLA typing with next generation sequencing should prove useful to select participants for prevention or intervention trials. The possible contribution of HLA-DRB3, -DRB4, and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 against either of the three amino acid variants R, W, or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respectively) at clinical diagnosis is unclear. Next-generation sequencing (NGS) was used to determine all DRB alleles in consecutively diagnosed patients ages 1-18 years with islet autoantibody-positive type 1 diabetes (n = 970) and control subjects (n = 448). DRB3, DRB4, or DRB5 alleles were tested for an association with the risk of DRB1 for autoantibodies, type 1 diabetes, or both. The association between type 1 diabetes and DRB1*03:01:01 was affected by DRB3*01:01:02 and DRB3*02:02:01. These DRB3 alleles were associated positively with GADA but negatively with ZnT8WA, IA-2A, and IAA. The negative association between type 1 diabetes and DRB1*13:01:01 was affected by DRB3*01:01:02 to increase the risk and by DRB3*02:02:01 to maintain a negative association. DRB4*01:03:01 was strongly associated with type 1 diabetes (P = 10-36), yet its association was extensively affected by DRB1 alleles from protective (DRB1*04:03:01) to high (DRB1*04:01:01) risk, but its association with DRB1*04:05:01 decreased the risk. HLA-DRB3, -DRB4, and -DRB5 affect type 1 diabetes risk and islet autoantibodies. HLA typing with NGS should prove useful to select participants for prevention or intervention trials. The possible contribution of HLA-DRB3, -DRB4, and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 against either of the three amino acid variants R, W, or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respectively) at clinical diagnosis is unclear. Next-generation sequencing (NGS) was used to determine all DRB alleles in consecutively diagnosed patients ages 1–18 years with islet autoantibody–positive type 1 diabetes (n = 970) and control subjects (n = 448). DRB3, DRB4, or DRB5 alleles were tested for an association with the risk of DRB1 for autoantibodies, type 1 diabetes, or both. The association between type 1 diabetes and DRB1*03:01:01 was affected by DRB3*01:01:02 and DRB3*02:02:01. These DRB3 alleles were associated positively with GADA but negatively with ZnT8WA, IA-2A, and IAA. The negative association between type 1 diabetes and DRB1*13:01:01 was affected by DRB3*01:01:02 to increase the risk and by DRB3*02:02:01 to maintain a negative association. DRB4*01:03:01 was strongly associated with type 1 diabetes (P = 10−36), yet its association was extensively affected by DRB1 alleles from protective (DRB1*04:03:01) to high (DRB1*04:01:01) risk, but its association with DRB1*04:05:01 decreased the risk. HLA-DRB3, -DRB4, and -DRB5 affect type 1 diabetes risk and islet autoantibodies. HLA typing with NGS should prove useful to select participants for prevention or intervention trials. The possible contribution of HLA-DRB3, -DRB4, and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 against either of the three amino acid variants R, W, or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respectively) at clinical diagnosis is unclear. Next-generation sequencing (NGS) was used to determine all DRB alleles in consecutively diagnosed patients ages 1-18 years with islet autoantibody-positive type 1 diabetes (n = 970) and control subjects (n = 448). DRB3, DRB4, or DRB5 alleles were tested for an association with the risk of DRB1 for autoantibodies, type 1 diabetes, or both. The association between type 1 diabetes and DRB1*03:01:01 was affected by DRB3*01:01:02 and DRB3*02:02:01. These DRB3 alleles were associated positively with GADA but negatively with ZnT8WA, IA-2A, and IAA. The negative association between type 1 diabetes and DRB1*13:01:01 was affected by DRB3*01:01:02 to increase the risk and by DRB3*02:02:01 to maintain a negative association. DRB4*01:03:01 was strongly associated with type 1 diabetes (P = 10(-36)), yet its association was extensively affected by DRB1 alleles from protective (DRB1*04:03:01) to high (DRB1*04:01:01) risk, but its association with DRB1*04:05:01 decreased the risk. HLA-DRB3, -DRB4, and -DRB5 affect type 1 diabetes risk and islet autoantibodies. HLA typing with NGS should prove useful to select participants for prevention or intervention trials.The possible contribution of HLA-DRB3, -DRB4, and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]), IA-2 antigen (IA-2A), or ZnT8 against either of the three amino acid variants R, W, or Q at position 325 (ZnT8RA, ZnT8WA, and ZnT8QA, respectively) at clinical diagnosis is unclear. Next-generation sequencing (NGS) was used to determine all DRB alleles in consecutively diagnosed patients ages 1-18 years with islet autoantibody-positive type 1 diabetes (n = 970) and control subjects (n = 448). DRB3, DRB4, or DRB5 alleles were tested for an association with the risk of DRB1 for autoantibodies, type 1 diabetes, or both. The association between type 1 diabetes and DRB1*03:01:01 was affected by DRB3*01:01:02 and DRB3*02:02:01. These DRB3 alleles were associated positively with GADA but negatively with ZnT8WA, IA-2A, and IAA. The negative association between type 1 diabetes and DRB1*13:01:01 was affected by DRB3*01:01:02 to increase the risk and by DRB3*02:02:01 to maintain a negative association. DRB4*01:03:01 was strongly associated with type 1 diabetes (P = 10(-36)), yet its association was extensively affected by DRB1 alleles from protective (DRB1*04:03:01) to high (DRB1*04:01:01) risk, but its association with DRB1*04:05:01 decreased the risk. HLA-DRB3, -DRB4, and -DRB5 affect type 1 diabetes risk and islet autoantibodies. HLA typing with NGS should prove useful to select participants for prevention or intervention trials. |
| Author | Persson, Martina Zhao, Michael Nelson, Wyatt C. Ivarsson, Sten A. Forsander, Gun Pyo, Chul-Woo Elding Larsson, Helena Zhao, Lue Ping Carlsson, Annelie Geraghty, Daniel E. Kockum, Ingrid Marcus, Claude Ludvigsson, Johnny Alshiekh, Shehab Samuelsson, Ulf Lernmark, Åke Örtqvist, Eva |
| Author_xml | – sequence: 1 givenname: Lue Ping surname: Zhao fullname: Zhao, Lue Ping organization: Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 2 givenname: Shehab surname: Alshiekh fullname: Alshiekh, Shehab organization: Department of Clinical Sciences, Lund University/Clinical Research Centre, Skåne University Hospital, Malmö, Sweden – sequence: 3 givenname: Michael surname: Zhao fullname: Zhao, Michael organization: Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 4 givenname: Annelie surname: Carlsson fullname: Carlsson, Annelie organization: Department of Pediatrics, Lund University, Lund, Sweden – sequence: 5 givenname: Helena surname: Elding Larsson fullname: Elding Larsson, Helena organization: Department of Clinical Sciences, Lund University/Clinical Research Centre, Skåne University Hospital, Malmö, Sweden – sequence: 6 givenname: Gun surname: Forsander fullname: Forsander, Gun organization: Department of Pediatrics, The Queen Silvia Children’s Hospital, Sahlgrenska University Hospital, Gothenburg, Sweden – sequence: 7 givenname: Sten A. surname: Ivarsson fullname: Ivarsson, Sten A. organization: Department of Clinical Sciences, Lund University/Clinical Research Centre, Skåne University Hospital, Malmö, Sweden – sequence: 8 givenname: Johnny surname: Ludvigsson fullname: Ludvigsson, Johnny organization: Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden – sequence: 9 givenname: Ingrid surname: Kockum fullname: Kockum, Ingrid organization: Department of Clinical Neurosciences, Karolinska Institutet, Solna, Sweden – sequence: 10 givenname: Claude surname: Marcus fullname: Marcus, Claude organization: Department of Clinical Science, Karolinska Institutet, Huddinge, Sweden – sequence: 11 givenname: Martina surname: Persson fullname: Persson, Martina organization: Department of Clinical Science, Karolinska Institutet, Huddinge, Sweden – sequence: 12 givenname: Ulf surname: Samuelsson fullname: Samuelsson, Ulf organization: Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden – sequence: 13 givenname: Eva surname: Örtqvist fullname: Örtqvist, Eva organization: Department of Women’s and Children’s Health, Karolinska Institutet, Solna, Sweden – sequence: 14 givenname: Chul-Woo surname: Pyo fullname: Pyo, Chul-Woo organization: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 15 givenname: Wyatt C. surname: Nelson fullname: Nelson, Wyatt C. organization: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 16 givenname: Daniel E. surname: Geraghty fullname: Geraghty, Daniel E. organization: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 17 givenname: Åke surname: Lernmark fullname: Lernmark, Åke organization: Department of Clinical Sciences, Lund University/Clinical Research Centre, Skåne University Hospital, Malmö, Sweden |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26740600$$D View this record in MEDLINE/PubMed https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-126246$$DView record from Swedish Publication Index https://lup.lub.lu.se/record/8592845$$DView record from Swedish Publication Index oai:portal.research.lu.se:publications/4e06c677-abf9-483d-956b-75a59056612e$$DView record from Swedish Publication Index http://kipublications.ki.se/Default.aspx?queryparsed=id:133041654$$DView record from Swedish Publication Index |
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| ContentType | Journal Article |
| Contributor | Forsberg, Maria Hemmingsson, Kristina Torbjörnsdotter, Torun Nilsson, Nils Östen Thåström, Anders Neiderud, Jan Ljungcrantz, Magnus Larsson, Karin Edvardsson, Stig Björsell, Britta Snellman, Kalle Gadd, Torsten Samuelsson, Ulf Åman, Jan Stenberg, Åke Larsson, Helena Elding Örtqvist, Eva Olivecrona, Anna Stjernstedt, Björn Enander, Rebecka Swenne, Ingemar Gundewall, Christer Åkesson, Karin Fureman, Anna-Lena Florell, Rein Hägg, Thomas Lundström, Göran Arvidsson, Carl-Göran Blomgren, Margareta Lundberg, Elena Hanås, Ragnar Jönsson, Björn Hellenberg, Lennart Tollig, Henrik Skogsberg, Lars Samuelsson, Bengt-Olof Wramner, Nils Brännström, Agneta Nordwall, Maria |
| Contributor_xml | – sequence: 1 givenname: Bengt-Olof surname: Samuelsson fullname: Samuelsson, Bengt-Olof – sequence: 2 givenname: Kalle surname: Snellman fullname: Snellman, Kalle – sequence: 3 givenname: Anna surname: Olivecrona fullname: Olivecrona, Anna – sequence: 4 givenname: Åke surname: Stenberg fullname: Stenberg, Åke – sequence: 5 givenname: Lars surname: Skogsberg fullname: Skogsberg, Lars – sequence: 6 givenname: Nils Östen surname: Nilsson fullname: Nilsson, Nils Östen – sequence: 7 givenname: Jan surname: Neiderud fullname: Neiderud, Jan – sequence: 8 givenname: Torun surname: Torbjörnsdotter fullname: Torbjörnsdotter, Torun – sequence: 9 givenname: Thomas surname: Hägg fullname: Hägg, Thomas – sequence: 10 givenname: Kristina surname: Hemmingsson fullname: Hemmingsson, Kristina – sequence: 11 givenname: Göran surname: Lundström fullname: Lundström, Göran – sequence: 12 givenname: Magnus surname: Ljungcrantz fullname: Ljungcrantz, Magnus – sequence: 13 givenname: Maria surname: Forsberg fullname: Forsberg, Maria – sequence: 14 givenname: Karin surname: Larsson fullname: Larsson, Karin – sequence: 15 givenname: Christer surname: Gundewall fullname: Gundewall, Christer – sequence: 16 givenname: Karin surname: Åkesson fullname: Åkesson, Karin – sequence: 17 givenname: Rebecka surname: Enander fullname: Enander, Rebecka – sequence: 18 givenname: Ulf surname: Samuelsson fullname: Samuelsson, Ulf – sequence: 19 givenname: Helena Elding surname: Larsson fullname: Larsson, Helena Elding – sequence: 20 givenname: Agneta surname: Brännström fullname: Brännström, Agneta – sequence: 21 givenname: Maria surname: Nordwall fullname: Nordwall, Maria – sequence: 22 givenname: Lennart surname: Hellenberg fullname: Hellenberg, Lennart – sequence: 23 givenname: Elena surname: Lundberg fullname: Lundberg, Elena – sequence: 24 givenname: Henrik surname: Tollig fullname: Tollig, Henrik – sequence: 25 givenname: Britta surname: Björsell fullname: Björsell, Britta – sequence: 26 givenname: Eva surname: Örtqvist fullname: Örtqvist, Eva – sequence: 27 givenname: Björn surname: Stjernstedt fullname: Stjernstedt, Björn – sequence: 28 givenname: Nils surname: Wramner fullname: Wramner, Nils – sequence: 29 givenname: Ragnar surname: Hanås fullname: Hanås, Ragnar – sequence: 30 givenname: Ingemar surname: Swenne fullname: Swenne, Ingemar – sequence: 31 givenname: Margareta surname: Blomgren fullname: Blomgren, Margareta – sequence: 32 givenname: Anders surname: Thåström fullname: Thåström, Anders – sequence: 33 givenname: Carl-Göran surname: Arvidsson fullname: Arvidsson, Carl-Göran – sequence: 34 givenname: Stig surname: Edvardsson fullname: Edvardsson, Stig – sequence: 35 givenname: Björn surname: Jönsson fullname: Jönsson, Björn – sequence: 36 givenname: Torsten surname: Gadd fullname: Gadd, Torsten – sequence: 37 givenname: Jan surname: Åman fullname: Åman, Jan – sequence: 38 givenname: Rein surname: Florell fullname: Florell, Rein – sequence: 39 givenname: Anna-Lena surname: Fureman fullname: Fureman, Anna-Lena |
| Copyright | 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. Copyright American Diabetes Association Mar 2016 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. 2016 |
| Copyright_xml | – notice: 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. – notice: Copyright American Diabetes Association Mar 2016 – notice: 2016 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. 2016 |
| CorporateAuthor | for the Better Diabetes Diagnosis (BDD) Study Group Better Diabetes Diagnosis (BDD) Study Group Pediatrik, Lund Section V Institutionen för kliniska vetenskaper, Lund Lunds universitet Profile areas and other strong research environments Department of Clinical Sciences, Malmö Lund University Sektion V Celiac Disease and Diabetes Unit Department of Clinical Sciences, Lund Strategiska forskningsområden (SFO) EXODIAB: Excellence of Diabetes Research in Sweden Faculty of Medicine Celiaki och diabetes Strategic research areas (SRA) Paediatrics (Lund) Medicinska fakulteten Pediatrisk endokrinologi Profilområden och andra starka forskningsmiljöer Institutionen för kliniska vetenskaper, Malmö Paediatric Endocrinology |
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Oct;9(5):460-72 – reference: 10553503 - Eur J Immunogenet. 1999 Oct;26(5):361-72 |
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| Snippet | The possible contribution of HLA-DRB3, -DRB4, and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]),... The possible contribution of HLA-DRB3 , -DRB4 , and -DRB5 alleles to type 1 diabetes risk and to insulin autoantibody (IAA), GAD65 (GAD autoantibody [GADA]),... The possible contribution of HLA-DRB3, -DRB4 and -DRB5 alleles to type 1 diabetes risk and to autoantibodies against insulin (IAA), GAD65 (GADA), IA-2 (IA-2A)... |
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| SubjectTerms | Adolescent Amino acids Antigens Autoantibodies - immunology Case-Control Studies Cation Transport Proteins - immunology Child Child, Preschool Clinical Medicine Diabetes Diabetes Mellitus, Type 1 - genetics Diabetes Mellitus, Type 1 - immunology Endocrinology and Diabetes Endokrinologi och diabetes Female Genetic Predisposition to Disease Glutamate Decarboxylase - immunology High-Throughput Nucleotide Sequencing HLA-DRB1 Chains - genetics HLA-DRB3 Chains - genetics HLA-DRB4 Chains - genetics HLA-DRB5 Chains - genetics Humans Immunoglobulins Immunology and Transplantation Infant Insulin Insulin - immunology Klinisk medicin Male Medical and Health Sciences Medicin och hälsovetenskap Odds Ratio Sequence Analysis, DNA Zinc Transporter 8 |
| Title | Next-Generation Sequencing Reveals That HLA-DRB3 , -DRB4 , and -DRB5 May Be Associated With Islet Autoantibodies and Risk for Childhood Type 1 Diabetes |
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