ArticleImmunogenetics1996
Peptide binding characteristics of the coeliac disease-associated DQ(alpha1*0501, beta1*0201) molecule.
Article in Immunogenetics, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 148 citations in OpenAlex.
- Tetramer visualization of gut-homing gluten-specific T cells in the peripheral blood of celiac disease patients.Proceedings of the National Academy of Sciences of the United States of America · 2007Trial
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- Assessment of Novel Proteins Triggering Celiac Disease via Docking-Based Approach.Molecules (Basel, Switzerland) · 2023Article
- Molecular and in vivo studies of a glutamate-class prolyl-endopeptidase for coeliac disease therapy.Nature communications · 2022Article
- Development of a Sequence Searchable Database of Celiac Disease-Associated Peptides and Proteins for Risk Assessment of Novel Food Proteins.Frontiers in allergy · 2022Article
- Gliadin Sequestration as a Novel Therapy for Celiac Disease: A Prospective Application for Polyphenols.International journal of molecular sciences · 2021Review
- Characterization of Human CD4 T Cells Specific for a C-Peptide/C-Peptide Hybrid Insulin Peptide.Frontiers in immunology · 2021Article
- Thermal and Acidic Treatments of Gluten Epitopes Affect Their Recognition by HLA-DQ2Frontiers in nutrition · 2021Article
- Influence of HLA-DQ2.5 Dose on Clinical Picture of Unrelated Celiac Disease Patients.Nutrients · 2020Article
- Coeliac Disease Pathogenesis: The Uncertainties of a Well-Known Immune Mediated Disorder.Frontiers in immunology · 2020Review
- The roles of MHC class II genes and post-translational modification in celiac disease.Immunogenetics · 2017Review
- Unraveling the structural basis for the unusually rich association of human leukocyte antigen DQ2.5 with class-II-associated invariant chain peptides.The Journal of biological chemistry · 2017Article
- The increased ability to present citrullinated peptides is not unique to HLA-SE molecules: arginine-to-citrulline conversion also enhances peptide affinity for HLA-DQ molecules.Arthritis research & therapy · 2016Article
- Type 1 diabetes associated HLA-DQ2 and DQ8 molecules are relatively resistant to HLA-DM mediated release of invariant chain-derived CLIP peptides.European journal of immunology · 2016Article
- Despite sequence homologies to gluten, salivary proline-rich proteins do not elicit immune responses central to the pathogenesis of celiac disease.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Different binding motifs of the celiac disease-associated HLA molecules DQ2.5, DQ2.2, and DQ7.5 revealed by relative quantitative proteomics of endogenous peptide repertoires.Immunogenetics · 2015Article
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- Targeted modification of wheat grain protein to reduce the content of celiac causing epitopes.Functional & integrative genomics · 2012Review
- The adaptive immune response in celiac disease.Seminars in immunopathology · 2012Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic susceptibility to coeliac disease (CD) is strongly associated with the expression of the HLA-DQ2 (alpha1(*)0501, beta1(*)0201) allele. There is evidence that this DQ2 molecule plays a role in the pathogenesis of CD as a restriction element for gliadin-specific T cells in the gut. However, it remains largely unclear which fragments of gliadin can actually be presented by the disease-associated DQ dimer. With a view to identifying possible CD-inducing antigens, we studied the peptide binding properties of DQ2. For this purpose, peptides bound to HLA-DQ2 were isolated and characterized. Dominant peptides were found to be derived from two self-proteins: in addition to several size-variants of the invariant chain (li)-derived CLIP peptide, a relatively large amount of an major histocompatibility complex (MHC) class I-derived peptide was found. Analogues of this naturally processed epitope (MHClalpha46 - 63) were tested in a cell-free peptide binding competition assay to investigate the requirements for binding to DQ2. First, a core sequence of 10 amino acids within the MHClalpha46 - 63 peptide was identified. By subsequent single amino acid substitution analysis of this core sequence, five putative anchor residues were identified at relative positions P1, P4, P6, P7, and P9. Replacement by the large, positively charged Lys at these positions resulted in a dramatic loss of binding. However, several other non-conservative substitutions had little or no discernable effect on the binding capacity of the peptides.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.