Research Article

Blocking Type I Interferon Signaling Rescues Lymphocytes from Oxidative Stress, Exhaustion, and Apoptosis in a Streptozotocin-Induced Mouse Model of Type I Diabetes

Figure 6

Lymphocytes from diabetic mice exhibit sustained phosphorylation of AKT, IκB-α, STAT1, and STAT2 during diabetes. PBMCs were isolated from five mice per group ( ) and were either stimulated with IFN-α (2000 IU/mL) for 5 minutes or left unstimulated. Cell lysates were then prepared for Western blot analysis. The immunoblots from one representative experiment of five independent experiments are shown for the phosphorylation of AKT, IκB-α, STAT1, and STAT2 (a, c, e, g). Total AKT, IκB-α, STAT1, and STAT2 were used as equal loading controls. The data acquired for five individuals per group are expressed as the normalized average of the phosphorylated protein to the total relevant protein SEM, as shown in (b, d, f, h). for unstimulated versus IFN-stimulated cells. The values for the level of normalized phosphoprotein in unstimulated cells were subtracted from those in IFN-stimulated cells to yield the specific phosphorylation values. The statistical analysis of the specific phosphorylation values revealed that * for diabetic versus control; # for diabetic + anti-IFNAR1 versus diabetic; + for diabetic + anti-IFNAR1 versus control.
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