Cellular Metabolism in B Cells in Type 1 Diabetes

Background/Objective: Type 1 diabetes (T1D) is an immune-mediated disease that results in the destruction of pancreatic beta cells. While cell classically considered T mediated, autoreactive B cells play important roles progression. depletion prevents non-obese diabetic (NOD) mice, and temporarily slows progression individuals with new-onset T1D. However, mechanisms function T1D are not fully known. Cellular metabolism has been shown to drive autoimmune development other mouse models. We hypothesize metabolic characteristics from NOD mice distinct non-autoimmune C57BL/6J (B6) mice; therefore, making cellular pathways viable targets for therapeutic intervention.
 Methods: Lymphocytes spleen, pancreas, lymph nodes, mesenteric/lumbar nodes were processed into single-cell suspensions. Glucose uptake was measured using fluorescent glucose analog 2-NBDG. Mitochondrial polarity probes mass membrane potential. Cells stained surface markers analyzed on Attune Nxt flow cytometer.
 Results: No statistically significant differences or mitochondrial lymphocyte subsets spleen PLNs B6 identified. In significantly higher pancreas compared PLNs. Polarity also non-specific mice.
 Conclusions/Impact: no lymphocytes ex vivo identified, future studies needed determine whether their activation drives alterations. Differences suggest influenced by islet microenvironment potential influence at site attack.