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Inflammation & Allergy-Drug Targets
(Formerly Current Drug Targets - Inflammation & Allergy)
ISSN (Print): 1871-5281
ISSN (Online): 2212-4055
DOI: 10.2174/187152811795564046      Price:  $58

NF-κB in Type 1 Diabetes

Author(s): Yuxing Zhao, Balasubramanian Krishnamurthy, Zia U.A. Mollah, Thomas W.H. Kay and Helen E. Thomas
Pages 208-217 (10)
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.
Type 1 diabetes, NF-κB, pancreatic beta cells, cytokine secretion, Islet transplantation, beta-cell destruction, insulitis, p65/RelA, RelB, p100/NF-B1, p105/NF-B2
St Vincent's Institute, 41 Victoria Parade, Fitzroy, Victoria, 3065, Melbourne, Australia.