Interferon alpha--a potential link in the pathogenesis of viral-induced type 1 diabetes and autoimmunity

The incidence of type 1 diabetes has been rapidly rising. Environmental factors such as viruses have been implicated as a possible agent accounting for this rise. Enteroviruses have recently been the focus in many research studies as a potential agent in the pathogenesis of type 1 diabetes. The mechanism of viral infection leading to beta cell destruction not only involves multiple pathways but also the cytokine-interferon alpha (IFN-alpha). Our hypothesis is that activation of toll receptors by double-stranded RNA or poly-IC (viral mimic) through induction of IFN-alpha may activate or accelerate immune-mediated beta cell destruction. Numerous clinical case reports have implicated that IFN-alpha therapy is associated with autoimmune diseases and that elevated serum IFN-alpha levels have been associated with type 1 diabetes. In multiple animal models, given specific genetic susceptibility, poly-IC can induce insulitis or diabetes. Therapeutic agents targeting IFN-alpha may potentially be beneficial in the prevention of type 1 diabetes and autoimmunity.