NF-κB in Type 1 Diabetes

Author(s): Yuxing Zhao, Balasubramanian Krishnamurthy, Zia U.A. Mollah, Thomas W.H. Kay, Helen E. Thomas

Journal Name: Inflammation & Allergy - Drug Targets (Discontinued)
Formerly Current Drug Targets - Inflammation & Allergy

Volume 10 , Issue 3 , 2011


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.

Keywords: 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

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Article Details

Year: 2011
Published on: 01 March, 2012
Page: [208 - 217]
Pages: 10
DOI: 10.2174/187152811795564046
Price: $65

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