Effect of anti-CD3 antibody treatment on islet transcriptomes in the nonobese diabetic (NOD) mouse model

Type 1 Diabetes (T1D) is a chronic autoimmune disease resulting from T cell-mediated destruction of pancreatic beta cells. Although T cells are known to destroy beta cells, how they may impact non-lethal forms of beta cell stress that also contribute to T1D development is not known. Here, we established an intermittent treatment regimen using a validated monoclonal anti-CD3 antibody on the female nonobese diabetic (NOD) mouse model for T1D at late prediabetic stages that leads to depletion of antigen-specific T cells and improvement of glucose tolerance. We used mRNA-seq to explore transcriptomic changes in isolated pancreatic islets from mice treated with anti-CD3 antibody or IgG as a control. Nine week old euglycemic female NOD mice were treated once per week for 4 weeks with IgG or anti-CD3 (2.5 mg/kg). Two or three days following the last dose of antibody, pancreatic islets were isolated from the mice and total RNA extracted using a Trizol-based kit approach. The total RNA was then submitted to a service provider for paired-end mRNA-seq on the Illumina platform.