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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.
Abstract Background The Jurkat cell line has an extensive history as a model of T cell signaling. But at the turn of the 21st century, some expression irregularities were observed, raising doubts about how closely the cell line paralleled normal human T cells. While numerous expression deficiencies have been described in Jurkat, genetic explanations have only been provided for a handful of defects.
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