JAK-STAT SIGNALING DRIVES AUTOIMMUNE DIABETES IN LEW.1WR1 RATS

Pancreatic islet cell populations in poly I:C + KRV-infected Ifnar1-/- LEW.1WR1 rats were compared to those of WT LEW.1WR1 rats to identify compensatory mechanism in endocrine cells that appear to lead to autoimmume diabetes in the infected Ifnar1-/- rats. Overall design: Pancreatic islet cells were extracted from LEW.1WR1 rats on Day 11 post-treatment under three conditions - PBS (no-treatment control), injections of polyinosine-polycytidylic acid (poly I:C) on days -3, -2, and -1 (no-KRV control), and poly I:C treatment followed by injection of KRV (Kilham rat virus) on day 0. For the poly IC+KRV treatment pancreatic islet cells were also extracted on days 7 and 9 post-treatment to observe the onset of insulitis over time. 10X single-cell RNA-Seq was performed on each sample and bioinformatic and imaging analysis was applied to identify the cell type subsets and identify the genes and spatial distribution of cells involved in the onset of autoimmune diabetes.