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Epitope Stealing as a Mechanism of Dominant Protection by HLA-DQ6 in Type 1 Diabetes
Molecular basis for increased susceptibility of Indigenous North Americans to seropositive rheumatoid arthritis
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
Crossreactivity to vinculin and microbes provides a molecular basis for HLA-based protection against rheumatoid arthritis
Type 1 Diabetes-associated HLA-DQ8 Transdimer Accommodates a Unique Peptide Repertoire
The type 1 diabetes associated HLA-DQ8-trans dimer accomodates a unique peptide repertoire
Gluten-Specific T Cells Cross-React between HLA-DQ8 and the HLA-DQ2 alpha/DQ8 beta Transdimer
Gluten-specific T cells cross-react between HLA-DQ8 and the HLA-DQ2α/DQ8β transdimer
Functional consequences of HLA-DQ8 homozygosity versus heterozygosity for islet autoimmunity in type 1 diabetes
Functional consequences of HLA-DQ8 homozygosity versus heterozygosity for islet autoimmunity in type 1 diabetes