These data suggest that both CS and hypoxia lead to increased oxidative stress and ROS/free radical production, which in turn induces auto-reactive pro-inflammatory T cell production, autoantibody generation (e.g., anti-dsDNA, anti-elastin and anti-RBC autoantibodies), enhanced transcriptional activation/expression of pro-inflammatory mediators (e.g., IL-6, IL-4, IL-8), and reduced expression of IFN-γ by promoting overactivation of NF-κB/APS and various epigenetic modifications. This evidence concerns the gene IL6 and autoimmune polyendocrinopathy.