Description
This study was performed to understand what controls the aggressivity of the pancreatic infiltrate during type-I diabetes development. We used the BDC2.5 transgenic mouse model. Samples were obtained at the age of onset of insultis. Depending on their genetic background, mice transgenic for the BDC2.5 T cell receptor present very different forms of insulitis. The NOD genetic background leads to a benign insulitis whereas the C57Bl/6-H2g7/g7 leads to an aggressive insulitis. We first studied how antigen-specific T cells are affected by these differences by obtaining the transcriptional profiles of BDC2.5 T cells from pancreas and pancreatic lymph nodes. We also compared the gene expression profiles of the entire leukocyte population present in the pancreatic lesion.