Pancreatic β-cell dysfunction in type 2 diabetes: Implications of inflammation and oxidative stress

Figure 2 An overview of the pathological mechanisms linking impaired immune function and inflammation during β-cell dysfunction in conditions of type 2 diabetes (characterized by hyperglycemia and hyperlipidemia). Briefly, CD4+ T cells can be activated by interleukin-12 produced from macrophages and dendritic cells, and this consequence occurs as part of a vicious process involving cytotoxic T cells and recruitment by the pancreatic islets. Notably, elevated levels of tumor necrosis factor-alpha are linked with activation of pro-inflammatory signals such as Janus kinase/signal transducer and activator of transcription that promote β-cell failure. IL-12: Interleukin-12; TNF-α: Tumor necrosis factor-alpha; INFs: Interferons; IAPP: Islet amyloid polypeptide; ROS: Reactive oxygen species; ER stress: Endoplasmic reticulum stress; JAK/STAT: Janus kinase/signal transducer and activator of transcription.