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| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | Eerligh, P. | en |
| dc.contributor.author | van Lummel, M. | en |
| dc.contributor.author | Zaldumbide, A. | en |
| dc.contributor.author | Moustakas, A. K. | en |
| dc.contributor.author | Duinkerken, G. | en |
| dc.contributor.author | Bondinas, G. | en |
| dc.contributor.author | Koeleman, B. P. | en |
| dc.contributor.author | Papadopoulos, G. K. | en |
| dc.contributor.author | Roep, B. O. | en |
| dc.date.accessioned | 2015-11-24T19:15:13Z | - |
| dc.date.available | 2015-11-24T19:15:13Z | - |
| dc.identifier.issn | 1476-5470 | - |
| dc.identifier.uri | https://olympias.lib.uoi.gr/jspui/handle/123456789/21478 | - |
| dc.rights | Default Licence | - |
| dc.subject | Adolescent | en |
| dc.subject | B-Lymphocytes/cytology/immunology | en |
| dc.subject | Diabetes Mellitus, Type 1/genetics/immunology/*metabolism | en |
| dc.subject | Epitopes, B-Lymphocyte/immunology | en |
| dc.subject | Genetic Predisposition to Disease | en |
| dc.subject | HLA-DQ Antigens/*genetics | en |
| dc.subject | Heterozygote | en |
| dc.subject | Homozygote | en |
| dc.subject | Humans | en |
| dc.subject | Insulin/genetics | en |
| dc.subject | Islets of Langerhans/*immunology | en |
| dc.subject | Male | en |
| dc.subject | Protein Binding | en |
| dc.subject | Syndecans/metabolism | en |
| dc.subject | T-Lymphocytes/cytology/immunology | en |
| dc.subject | Thymosin/metabolism | en |
| dc.title | Functional consequences of HLA-DQ8 homozygosity versus heterozygosity for islet autoimmunity in type 1 diabetes | en |
| heal.type | journalArticle | - |
| heal.type.en | Journal article | en |
| heal.type.el | Άρθρο Περιοδικού | el |
| heal.identifier.primary | 10.1038/gene.2011.24 | - |
| heal.identifier.secondary | http://www.ncbi.nlm.nih.gov/pubmed/21562577 | - |
| heal.language | en | - |
| heal.access | campus | - |
| heal.recordProvider | Πανεπιστήμιο Ιωαννίνων. Σχολή Επιστημών Υγείας. Τμήμα Ιατρικής | el |
| heal.publicationDate | 2011 | - |
| heal.abstract | Human leukocyte antigen (HLA) class II haplotypes are established risk factors in type 1 diabetes (T1D). The heterozygous DQ2/8 genotype confers the highest risk, whereas the DQ6/8 genotype is protective. We hypothesized that DQ2/8 trans-molecules composed of alpha and beta chains from DQ2 and DQ8 express unique beta-cell epitopes, whereas DQ6 may interfere with peptide binding to DQ8. Here we show that a single insulin epitope (InsB13-21) within the T1D prototype antigenic InsB6-22 peptide can bind to both cis- and trans-dimers, although these molecules display different peptide binding patterns. DQ6 binds a distinct insulin epitope (InsB6-14). The phenotype of DQ8-restricted T cells from a T1D patient changed from proinflammatory to anti-inflammatory in the presence of DQ6. Our data provide new insights into both susceptible and protective mechanism of DQ, where protecting HLA molecules bind autoantigens in a different (competing) binding register leading to 'epitope stealing', thereby inducing a regulatory, rather than a pathogenic immune response. | en |
| heal.journalName | Genes Immun | en |
| heal.journalType | peer-reviewed | - |
| heal.fullTextAvailability | TRUE | - |
| Appears in Collections: | Άρθρα σε επιστημονικά περιοδικά ( Ανοικτά) - ΙΑΤ | |
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