Abstract
Type 1 diabetes (T1D) is characterized by a selective destruction of insulin producing pancreatic beta cells, by the immune system. During the autoimmune assault, pro-inflammatory cytokines, such as interleukin (IL)-1b, tumour necrosis factor (TNF)-a and interferon (IFN)-g contribute for beta cells death, manly via NF-kB activation. Since NF-kB is a key regulator of several cellular respo…