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Insulin peptide recognition by early diabetogenic T cells Type 1 diabetes is initiated by loss of T cell tolerance to pancreatic islet autoantigens including insulin. Gioia et al. developed peptide-MHC tetramer reagents capable of distinguishing separate populations of insulin-reactive CD4+ T cells from diabetes-prone NOD mice that differ in the register used for insulin peptide binding to class II MHC.
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