Type 1 diabetes is an autoimmune disease in which pancreatic beta cells are destroyed by autoreactive T cells. It is a common pediatric disease with increasing incidence. Islet transplantation may be a therapeutic option, however, the current limitations of this procedure mean that for most sufferers of type 1 diabetes there is no cure. The transcription factor NF-κB has been widely studied for its role in development of type 1 diabetes. Recent data have shown that NF-κB is required for activation of autoreactive T cells, and its hyperactivity in monocytes and dendritic cells results in altered cytokine secretion and antigen presentation, which ultimately contributes to the initiation of type 1 diabetes. NF-κB is also activated by a number of proinflammatory cytokines to regulate both the survival and death of beta cells. The critical role of NF-κB in type 1 diabetes renders it a promising pharmaceutical target in the intervention of this disease and further understanding of the NF-κB pathway will have an important implication on the development of novel and safe therapeutic strategies.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2174/187152811795564046 | DOI Listing |
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!