ArticleEuropean journal of immunology2016
Type 1 diabetes associated HLA-DQ2 and DQ8 molecules are relatively resistant to HLA-DM mediated release of invariant chain-derived CLIP peptides.
Article in European journal of immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Autologous fecal microbiota capsules are safe and potentially preserve beta-cell function in individuals with type 1 diabetes.Gut microbes · 2025Trial
- Structural Modulation and Binding of HLA-DQ8 by Cysteine-to-Serine Mutated Insulin Peptide: Insights from Molecular Dynamics Simulations.International journal of molecular sciences · 2026Article
- Identification of a type 1 diabetes-associated T cell receptor repertoire signature from the human peripheral blood.Science advances · 2026Article
- Article
- Sex as a modifier of genetic risk for type 1 diabetes.Diabetes, obesity & metabolism · 2025Review
- Persisting plasma proinsulin levels in a cohort of 482 individuals with long-standing type 1 diabetes mellitus.Diabetes, obesity & metabolism · 2025Article
- Two DRB3 residues predictively associate with the progression to type 1 diabetes among DR3 carriers.JCI insight · 2025Article
- Peripheral blood gene expression stratifies rate of progression to type 1 diabetes in autoantibody-positive children in the TEDDY study.Frontiers in immunology · 2025Article
- Review
- The MHC Class II Antigen-Processing and Presentation Pathway Is Dysregulated in Type 1 Diabetes.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Prediction of celiac disease associated epitopes and motifs in a protein.Frontiers in immunology · 2023Article
- Protective HLA alleles against severe COVID-19: HLA-A*68 as an ancestral protection allele in Tapachula-Chiapas, Mexico.Clinical immunology (Orlando, Fla.) · 2022Article
- Production of Class II MHC Proteins in Lentiviral Vector-Transduced HEK-293T Cells for Tetramer Staining Reagents.Current protocols · 2021Article
- T-Cell Epitopes and Neo-epitopes in Type 1 Diabetes: A Comprehensive Update and Reappraisal.Diabetes · 2020Article
- HLA-DM catalytically enhances peptide dissociation by sensing peptide-MHC class II interactions throughout the peptide-binding cleft.The Journal of biological chemistry · 2020Article
- Distinct editing functions of natural HLA-DM allotypes impact antigen presentation and CD4Cellular & molecular immunology · 2020Article
- Epitope Selection for HLA-DQ2 Presentation: Implications for Celiac Disease and Viral Defense.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Class II MHC antigen processing in immune tolerance and inflammation.Immunogenetics · 2019Review
- Rapid CLIP dissociation from MHC II promotes an unusual antigen presentation pathway in autoimmunity.The Journal of experimental medicine · 2018Article
- 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
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
HLA-DM is essential for editing peptides bound to MHC class II, thus influencing the repertoire of peptides mediating selection and activation of CD4(+) T cells. Individuals expressing HLA-DQ2 or DQ8, and DQ2/8 trans-dimers, have elevated risk for type 1 diabetes (T1D). Cells coexpressing DM with these DQ molecules were observed to express elevated levels of CLIP (Class II associated invariant chain peptide). Relative resistance to DM-mediated editing of CLIP was further confirmed by HPLC-MS/MS analysis of eluted peptides, which also demonstrated peptides from known T1D-associated autoantigens, including a shared epitope from ZnT8 that is presented by all four major T1D-susceptible DQ molecules. Assays with purified recombinant soluble proteins confirmed that DQ2-CLIP complexes are highly resistant to DM editing, whereas DQ8-CLIP is partially sensitive to DM, but with an apparent reduction in catalytic potency. DM sensitivity was enhanced in mutant DQ8 molecules with disruption of hydrogen bonds that stabilize DQ8 near the DM-binding region. Our findings show that T1D-susceptible DQ2 and DQ8 share significant resistance to DM editing, compared with control DQ molecules. The relative resistance of the T1D-susceptible DQ molecules to DM editing and preferential presentation of T1D-associated autoantigenic peptides may contribute to the pathogenesis of T1D.
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