Next-Generation HLA Sequence Analysis Uncovers Seven HLA-DQ Amino Acid Residues and Six Motifs Resistant to Childhood Type 1 Diabetes
HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (αa1, α157, α196, β9, β30, β57, and β70) that are resistant to T1D...
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| Published in | Diabetes (New York, N.Y.) Vol. 69; no. 11; pp. 2523 - 2535 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Diabetes Association
01.11.2020
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 0012-1797 1939-327X 1939-327X |
| DOI | 10.2337/db20-0374 |
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| Abstract | HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (αa1, α157, α196, β9, β30, β57, and β70) that are resistant to T1D among subjects with DQ4-, 5-, 6-, and 7-resistant DQ haplotypes. These 7 residues form 13 common motifs: 6 motifs are significantly resistant, 6 motifs have modest or no associations (P values >0.05), and 1 motif has 7 copies observed among control subjects only. The motifs “DAAFYDG,” “DAAYHDG,” and “DAAYYDR” have significant resistance to T1D (odds ratios [ORs] 0.03, 0.25, and 0.18; P = 6.11 × 10−24, 3.54 × 10−15, and 1.03 × 10−21, respectively). Remarkably, a change of a single residue from the motif “DAAYHDG” to “DAAYHSG” (D to S at β57) alters the resistance potential, from resistant motif (OR 0.15; P = 3.54 × 10−15) to a neutral motif (P = 0.183), the change of which was significant (Fisher P value = 0.0065). The extended set of linked residues associated with T1D resistance and unique to each cluster of HLA-DQ haplotypes represents facets of all known features and functions of these molecules: antigenic peptide binding, peptide–MHC class II complex stability, β167-169 RGD loop, T-cell receptor binding, formation of homodimer of α-β heterodimers, and cholesterol binding in the cell membrane rafts. Identification of these residues is a novel understanding of resistant DQ associations with T1D. Our analyses endow potential molecular approaches to identify immunological mechanisms that control disease susceptibility or resistance to provide novel targets for immunotherapeutic strategies. |
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| AbstractList | HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (αa1, α157, α196, β9, β30, β57, and β70) that are resistant to T1D among subjects with DQ4-, 5-, 6-, and
-resistant DQ haplotypes. These 7 residues form 13 common motifs: 6 motifs are significantly resistant, 6 motifs have modest or no associations (
values >0.05), and 1 motif has 7 copies observed among control subjects only. The motifs "DAAFYDG," "DAAYHDG," and "DAAYYDR" have significant resistance to T1D (odds ratios [ORs] 0.03, 0.25, and 0.18;
= 6.11 × 10
, 3.54 × 10
, and 1.03 × 10
, respectively). Remarkably, a change of a single residue from the motif "DAAYHDG" to "DAAYHSG" (D to S at β57) alters the resistance potential, from resistant motif (OR 0.15;
= 3.54 × 10
) to a neutral motif (
= 0.183), the change of which was significant (Fisher
value = 0.0065). The extended set of linked residues associated with T1D resistance and unique to each cluster of HLA-DQ haplotypes represents facets of all known features and functions of these molecules: antigenic peptide binding, peptide-MHC class II complex stability, β167-169 RGD loop, T-cell receptor binding, formation of homodimer of α-β heterodimers, and cholesterol binding in the cell membrane rafts. Identification of these residues is a novel understanding of resistant DQ associations with T1D. Our analyses endow potential molecular approaches to identify immunological mechanisms that control disease susceptibility or resistance to provide novel targets for immunotherapeutic strategies. HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (αa1, α157, α196, β9, β30, β57, β70) that are resistant to T1D among subjects with DQ4, 5, 6 and 7 resistant DQ haplotypes. These seven residues form 13 common motifs; six motifs are significantly resistant, six motifs have modest or no associations (p-values>0.05), and one motif has 7 copies observed among controls only. The motif "DAAFYDG", "DAAYHDG" and "DAAYYDR" have significant resistance to T1D (OR = 0.03, 0.25 and 0.18, p-value = 6.11*10-24, 3.54*10-15 and 1.03*10-21, respectively). Remarkably, a change of a single residue from the motif "DAAYH D G" to "DAAYH S G" (D to S at β57) alters the resistance potential, from resistant motif (OR = 0.15, p-value = 3.54*10-15) to a neutral motif (p-value = 0.183), the change of which was significant (Fisher's p-value = 0.0065). Theextended set of linked residues associated with T1D resistance and unique to each cluster of HLA-DQ haplotypes represents facets of all known features and functions of these molecules: antigenic peptide binding, pMHCII complex stability, β167-169 RGD loop, TCR binding, formation of homodimer of alpha-beta heterodimers, and cholesterol binding in the cell membrane rafts. Identifications of these residues is a novel understanding of resistant DQ associations with T1D. Our analyses endow potential molecular approaches to identify immunological mechanisms that control disease susceptibility or resistance to provide novel targets for immunotherapeutic strategies. HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (αa1, α157, α196, β9, β30, β57, and β70) that are resistant to T1D among subjects with DQ4-, 5-, 6-, and 7-resistant DQ haplotypes. These 7 residues form 13 common motifs: 6 motifs are significantly resistant, 6 motifs have modest or no associations (P values >0.05), and 1 motif has 7 copies observed among control subjects only. The motifs “DAAFYDG,” “DAAYHDG,” and “DAAYYDR” have significant resistance to T1D (odds ratios [ORs] 0.03, 0.25, and 0.18; P = 6.11 × 10−24, 3.54 × 10−15, and 1.03 × 10−21, respectively). Remarkably, a change of a single residue from the motif “DAAYHDG” to “DAAYHSG” (D to S at β57) alters the resistance potential, from resistant motif (OR 0.15; P = 3.54 × 10−15) to a neutral motif (P = 0.183), the change of which was significant (Fisher P value = 0.0065). The extended set of linked residues associated with T1D resistance and unique to each cluster of HLA-DQ haplotypes represents facets of all known features and functions of these molecules: antigenic peptide binding, peptide–MHC class II complex stability, β167-169 RGD loop, T-cell receptor binding, formation of homodimer of α-β heterodimers, and cholesterol binding in the cell membrane rafts. Identification of these residues is a novel understanding of resistant DQ associations with T1D. Our analyses endow potential molecular approaches to identify immunological mechanisms that control disease susceptibility or resistance to provide novel targets for immunotherapeutic strategies. HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (alpha a1, alpha 157, alpha 196, beta 9, beta 30, beta 57, and beta 70) that are resistant to T1D among subjects with DQ4-, 5-, 6-, and7-resistant DQ haplotypes. These 7 residues form 13 common motifs: 6 motifs are significantly resistant, 6 motifs have modest or no associations (Pvalues >0.05), and 1 motif has 7 copies observed among control subjects only. The motifs "DAAFYDG," "DAAYHDG," and "DAAYYDR" have significant resistance to T1D (odds ratios [ORs] 0.03, 0.25, and 0.18;P= 6.11 x 10(-24), 3.54 x 10(-15), and 1.03 x 10(-21), respectively). Remarkably, a change of a single residue from the motif "DAAYHDG" to "DAAYHSG" (D to S at beta 57) alters the resistance potential, from resistant motif (OR 0.15;P= 3.54 x 10(-15)) to a neutral motif (P= 0.183), the change of which was significant (FisherPvalue = 0.0065). The extended set of linked residues associated with T1D resistance and unique to each cluster of HLA-DQ haplotypes represents facets of all known features and functions of these molecules: antigenic peptide binding, peptide-MHC class II complex stability, beta 167-169 RGD loop, T-cell receptor binding, formation of homodimer of alpha-beta heterodimers, and cholesterol binding in the cell membrane rafts. Identification of these residues is a novel understanding of resistant DQ associations with T1D. Our analyses endow potential molecular approaches to identify immunological mechanisms that control disease susceptibility or resistance to provide novel targets for immunotherapeutic strategies. HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (αa1, α157, α196, β9, β30, β57, and β70) that are resistant to T1D among subjects with DQ4-, 5-, 6-, and 7-resistant DQ haplotypes. These 7 residues form 13 common motifs: 6 motifs are significantly resistant, 6 motifs have modest or no associations (P values >0.05), and 1 motif has 7 copies observed among control subjects only. The motifs "DAAFYDG," "DAAYHDG," and "DAAYYDR" have significant resistance to T1D (odds ratios [ORs] 0.03, 0.25, and 0.18; P = 6.11 × 10-24, 3.54 × 10-15, and 1.03 × 10-21, respectively). Remarkably, a change of a single residue from the motif "DAAYHDG" to "DAAYHSG" (D to S at β57) alters the resistance potential, from resistant motif (OR 0.15; P = 3.54 × 10-15) to a neutral motif (P = 0.183), the change of which was significant (Fisher P value = 0.0065). The extended set of linked residues associated with T1D resistance and unique to each cluster of HLA-DQ haplotypes represents facets of all known features and functions of these molecules: antigenic peptide binding, peptide-MHC class II complex stability, β167-169 RGD loop, T-cell receptor binding, formation of homodimer of α-β heterodimers, and cholesterol binding in the cell membrane rafts. Identification of these residues is a novel understanding of resistant DQ associations with T1D. Our analyses endow potential molecular approaches to identify immunological mechanisms that control disease susceptibility or resistance to provide novel targets for immunotherapeutic strategies.HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on high-risk HLA-DQ2.5 and DQ8.1, the current analysis uncovers seven residues (αa1, α157, α196, β9, β30, β57, and β70) that are resistant to T1D among subjects with DQ4-, 5-, 6-, and 7-resistant DQ haplotypes. These 7 residues form 13 common motifs: 6 motifs are significantly resistant, 6 motifs have modest or no associations (P values >0.05), and 1 motif has 7 copies observed among control subjects only. The motifs "DAAFYDG," "DAAYHDG," and "DAAYYDR" have significant resistance to T1D (odds ratios [ORs] 0.03, 0.25, and 0.18; P = 6.11 × 10-24, 3.54 × 10-15, and 1.03 × 10-21, respectively). Remarkably, a change of a single residue from the motif "DAAYHDG" to "DAAYHSG" (D to S at β57) alters the resistance potential, from resistant motif (OR 0.15; P = 3.54 × 10-15) to a neutral motif (P = 0.183), the change of which was significant (Fisher P value = 0.0065). The extended set of linked residues associated with T1D resistance and unique to each cluster of HLA-DQ haplotypes represents facets of all known features and functions of these molecules: antigenic peptide binding, peptide-MHC class II complex stability, β167-169 RGD loop, T-cell receptor binding, formation of homodimer of α-β heterodimers, and cholesterol binding in the cell membrane rafts. Identification of these residues is a novel understanding of resistant DQ associations with T1D. Our analyses endow potential molecular approaches to identify immunological mechanisms that control disease susceptibility or resistance to provide novel targets for immunotherapeutic strategies. |
| Author | Nelson, Wyatt C. Pyo, Chul-Woo Elding Larsson, Helena Zhao, Lue Ping Papadopoulos, George K. Carlsson, Annelie Geraghty, Daniel E. Wang, Ruihan Moustakas, Antonis K. Marcus, Claude Kwok, William W. Ludvigsson, Johnny Samuelsson, Ulf Bondinas, George P. Lernmark, Åke |
| Author_xml | – sequence: 1 givenname: Lue Ping orcidid: 0000-0002-1387-7165 surname: Zhao fullname: Zhao, Lue Ping organization: Public Health Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 2 givenname: George K. orcidid: 0000-0002-6944-6591 surname: Papadopoulos fullname: Papadopoulos, George K. organization: Laboratory of Biophysics, Biochemistry, Biomaterials and Bioprocessing, Faculty of Agricultural Technology, Technological Educational Institute of Epirus, Arta, Greece – sequence: 3 givenname: William W. surname: Kwok fullname: Kwok, William W. organization: Benaroya Research Institute at Virginia Mason, Seattle, WA – sequence: 4 givenname: Antonis K. surname: Moustakas fullname: Moustakas, Antonis K. organization: Department of Food Science and Technology, Faculty of Environment, Ionian University, Argostoli, Cephalonia, Greece – sequence: 5 givenname: George P. surname: Bondinas fullname: Bondinas, George P. organization: Laboratory of Biophysics, Biochemistry, Biomaterials and Bioprocessing, Faculty of Agricultural Technology, Technological Educational Institute of Epirus, Arta, Greece – sequence: 6 givenname: Annelie surname: Carlsson fullname: Carlsson, Annelie organization: Department of Pediatrics, Lund University, Lund, Sweden – sequence: 7 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: 8 givenname: Johnny surname: Ludvigsson fullname: Ludvigsson, Johnny organization: Crown Princess Victoria Children’s Hospital and Division of Pediatrics, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden – sequence: 9 givenname: Claude surname: Marcus fullname: Marcus, Claude organization: Division of Pediatrics, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden – sequence: 10 givenname: Ulf surname: Samuelsson fullname: Samuelsson, Ulf organization: Crown Princess Victoria Children’s Hospital and Division of Pediatrics, Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden – sequence: 11 givenname: Ruihan surname: Wang fullname: Wang, Ruihan organization: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 12 givenname: Chul-Woo surname: Pyo fullname: Pyo, Chul-Woo organization: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 13 givenname: Wyatt C. surname: Nelson fullname: Nelson, Wyatt C. organization: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 14 givenname: Daniel E. surname: Geraghty fullname: Geraghty, Daniel E. organization: Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, WA – sequence: 15 givenname: Åke orcidid: 0000-0003-1735-0499 surname: Lernmark fullname: Lernmark, Åke organization: Department of Clinical Sciences, Lund University Clinical Research Centre, Skåne University Hospital, Malmö, Sweden |
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| Copyright | 2020 by the American Diabetes Association. Copyright American Diabetes Association Nov 1, 2020 2020 by the American Diabetes Association 2020 |
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| CorporateAuthor | 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 Pediatric Autoimmunity 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 autoimmunitet Profilområden och andra starka forskningsmiljöer Pediatrisk endokrinologi Institutionen för kliniska vetenskaper, Malmö Paediatric Endocrinology |
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| PublicationPlace_xml | – name: United States – name: New York |
| PublicationTitle | Diabetes (New York, N.Y.) |
| PublicationTitleAlternate | Diabetes |
| PublicationYear | 2020 |
| Publisher | American Diabetes Association |
| Publisher_xml | – name: American Diabetes Association |
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Members of the Swedish Childhood Diabetes Study publication-title: Diabetes doi: 10.2337/diab.44.1.125 |
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| Snippet | HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow up on the earlier analysis on... HLA-DQA1 and -DQB1 genes have significant and potentially causal associations with autoimmune type 1 diabetes (T1D). To follow on the earlier analysis on... |
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| SubjectTerms | Amino Acid Motifs - genetics Amino Acid Sequence Cell membranes Childhood Children Cholesterol Clinical Medicine Diabetes Diabetes mellitus (insulin dependent) Diabetes Mellitus, Type 1 - genetics Disease resistance DQA1 protein Endocrinology and Diabetes Endokrinologi och diabetes Gene Expression Regulation Genetic Predisposition to Disease Genetics/Genomes/Proteomics/Metabolomics Haplotypes High-Throughput Nucleotide Sequencing - methods Histocompatibility antigen HLA HLA-DQ Antigens - genetics HLA-DQ Antigens - metabolism Humans Klinisk medicin Lipid rafts Lymphocytes T Major histocompatibility complex Medical and Health Sciences Medicin och hälsovetenskap Models, Molecular Peptides Protein Conformation Sequence analysis T cell receptors |
| Title | Next-Generation HLA Sequence Analysis Uncovers Seven HLA-DQ Amino Acid Residues and Six Motifs Resistant to Childhood Type 1 Diabetes |
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