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- W1565459943 abstract "Abstract Homozygous HLA-DQ2, 8 or heterozygous 2/8 are highly associated with developing Type-1 diabetes (T1D), but the underlining molecular mechanism is not clear. HLA-DM is essential for editing peptides bound to MHC-II, thus influencing the repertoire of peptides presented by APCs, with potential impact on selection/activation of CD4+ T cells. We hypothesized that unique properties of T1D associated DQs, including different binding affinity for CLIP or other peptides & different sensitivity to DM editing, might confer high risk of T1D. Higher CLIP levels were found on the surface of DQ2+, 8+ or 2/8+ cells, compared to T1D protective DQ6+ cells, indicating a relative resistance to DM editing. HPLC-MS/MS analysis of eluted peptides from DQs showed that CLIPs containing longer N-terminal tails & more long peptides (>20 aa) were loaded on DQ2, 8 or 2/8, compared to DQ6. Among eluted peptides, several were derived from known auto-Ag identified in T1D. Peptide binding motifs of DQ2, 8 & 2/8 were different from DQ6, but similar to that of DQ8 as previously reported. Furthermore, DQ peptide binding assay demonstrated that CLIP2 had higher relative binding affinity to DQ2, 8 or 2/8, compared to DQ6. Disruption of hydrogen bonds near P1 pocket in DQ8 reversed its DM editing resistance. Collectively, our results showed that the DM sensitivity of DQ2, 8 & 2/8 is lower than that of DQ6. The relative resistance to DM editing of the T1D associated DQs may contribute to the pathogenesis of T1D." @default.
- W1565459943 created "2016-06-24" @default.
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- W1565459943 date "2014-05-01" @default.
- W1565459943 modified "2023-09-27" @default.
- W1565459943 title "Relative resistance to HLA-DM editing is a distinguishing characteristic of Type-1 diabetes associated HLA-DQ molecules (APP2P.100)" @default.
- W1565459943 doi "https://doi.org/10.4049/jimmunol.192.supp.43.1" @default.
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