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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Vydané v:Diabetes (New York, N.Y.) Ročník 65; číslo 3; s. 710
Hlavní autori: Zhao, Lue Ping, Alshiekh, Shehab, Zhao, Michael, Carlsson, Annelie, Larsson, Helena Elding, Forsander, Gun, Ivarsson, Sten A, Ludvigsson, Johnny, Kockum, Ingrid, Marcus, Claude, Persson, Martina, Samuelsson, Ulf, Örtqvist, Eva, Pyo, Chul-Woo, Nelson, Wyatt C, Geraghty, Daniel E, Lernmark, Åke
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: United States 01.03.2016
Predmet:
Adolescent
Autoantibodies - immunology
Case-Control Studies
Cation Transport Proteins - immunology
Child
Child, Preschool
Diabetes Mellitus, Type 1 - genetics
Diabetes Mellitus, Type 1 - immunology
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
Infant
Insulin - immunology
Male
Odds Ratio
Sequence Analysis, DNA
Zinc Transporter 8
ISSN:1939-327X, 1939-327X
On-line prístup:Zistit podrobnosti o prístupe
Tagy: Pridať tag
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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 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
Forsander, Gun
Pyo, Chul-Woo
Zhao, Lue Ping
Ivarsson, Sten A
Carlsson, Annelie
Geraghty, Daniel E
Kockum, Ingrid
Marcus, Claude
Ludvigsson, Johnny
Alshiekh, Shehab
Samuelsson, Ulf
Larsson, Helena Elding
Lernmark, Åke
Örtqvist, Eva
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/26740600$$D View this record in MEDLINE/PubMed
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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
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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.
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License 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.
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PublicationTitle Diabetes (New York, N.Y.)
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– reference: 10426387 - Diabetes. 1999 Aug;48(8):1658-61
– reference: 19922436 - J Thromb Haemost. 2010 Feb;8(2):257-62
– reference: 17130525 - Ann N Y Acad Sci. 2006 Oct;1079:1-8
– reference: 11079747 - Diabetologia. 2000 Oct;43(10):1282-92
– reference: 19369670 - N Engl J Med. 2009 Apr 16;360(16):1646-54
– reference: 23462545 - Diabetes. 2013 Jul;62(7):2618-22
– reference: 21564455 - Pediatr Diabetes. 2011 Dec;12(8):733-43
– reference: 9562346 - Diabetologia. 1998 Apr;41(4):424-9
– reference: 19140825 - Tissue Antigens. 2009 Feb;73(2):95-170
– reference: 16186404 - Diabetes. 2005 Oct;54(10):2995-3001
– reference: 21244337 - Autoimmunity. 2011 Aug;44(5):394-405
– reference: 23052709 - Genes Immun. 2012 Dec;13(8):632-40
– reference: 20337975 - Pediatr Diabetes. 2010 Dec;11(8):513-20
– reference: 21169359 - J Biol Chem. 2011 Mar 4;286(9):6989-98
– reference: 25167774 - Hum Immunol. 2014 Oct;75(10):1040-6
– reference: 22787139 - Diabetes. 2012 Oct;61(10):2556-64
– reference: 11791212 - Am J Hum Genet. 2002 Feb;70(2):425-34
– reference: 26027777 - Hum Immunol. 2015 Dec;76(12):928-38
– reference: 23835325 - Diabetes. 2013 Oct;62(10):3636-40
– reference: 21712811 - Int J Obes (Lond). 2012 May;36(5):718-24
– reference: 24206368 - Pediatr Diabetes. 2014 Aug;15(5):336-44
– reference: 10331157 - Eur J Immunogenet. 1999 Apr-Jun;26(2-3):117-27
– reference: 19429597 - J Med Genet. 2009 Jul;46(7):469-71
– reference: 21708156 - J Immunol Methods. 2011 Aug 31;371(1-2):25-37
– reference: 23762245 - PLoS One. 2013;8(6):e64683
– reference: 10209508 - Clin Exp Immunol. 1999 Apr;116(1):78-83
– reference: 24357215 - Diabetes Care. 2014 Jan;37 Suppl 1:S81-90
– reference: 11978629 - Diabetes. 2002 May;51(5):1346-55
– reference: 22278338 - Diabetologia. 2012 Apr;55(4):996-1000
– reference: 18252895 - Diabetes. 2008 Apr;57(4):1084-92
– reference: 25660258 - Diabetologia. 2015 May;58(5):980-7
– reference: 19430480 - Nat Genet. 2009 Jun;41(6):703-7
– reference: 11433380 - Eur J Immunol. 2001 Jun;31(6):1837-46
– reference: 17931054 - Diabetes Technol Ther. 2007 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]),...
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SubjectTerms Adolescent
Autoantibodies - immunology
Case-Control Studies
Cation Transport Proteins - immunology
Child
Child, Preschool
Diabetes Mellitus, Type 1 - genetics
Diabetes Mellitus, Type 1 - immunology
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
Infant
Insulin - immunology
Male
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
URI https://www.ncbi.nlm.nih.gov/pubmed/26740600
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