Inflammatory profile of NOD.Batf3-/- islets

NOD mice deficient in the transcription factor Batf3 never develop diabetes. The goal of this study was to determine if NOD.Batf3-/- mice islets had any inflammatory signature associated with type 1 diabetes. Islets of Langerhans were isolated from NOD, NOD.Batf3-/-, and NOD.Rag1-/- and then compared to determine inflammatory gene profiles. At 6 and 8 weeks of age, NOD.Batf3-/- islets had an absence of inflammatory gene expression and were almost identical to uninflamed NOD.Rag1-/- islets. This work shows that absence of the Batf3 transcription factor is sufficient to prevent all the inflammatory sequelae of autoimmune diabetes. RNA was isolated from the pancreatic islets of Langerhans of 27 experimental mice. Mice were aged either 6 or 8 weeks. Three genotypes were tested: NOD, NOD.Rag1-/-, and NOD.Batf3-/-. There were 3-6 biological replicates per condition. All mice were female. All data was normalized using RMA in Arraystar.