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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >NF-kappa B prevents beta cell death and autoimmune diabetes in NOD mice
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NF-kappa B prevents beta cell death and autoimmune diabetes in NOD mice

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摘要

Whereas NF-kappa B has potent antiapoptotic function in most cell types, it was reported that in pancreatic 13 cells it serves a proapoptotic function and may contribute to the pathogenesis of autoimmune type 1 diabetes. To investigate the role of beta cell NF-kappa B in autoimmune diabetes, we produced transgenic mice expressing a nondegradable form of l kappa B alpha in pancreatic 13 cells (RIP-ml kappa B alpha mice). 13 cells of these mice were more susceptible to killing by TNF-alpha plus IFN-gamma but more resistant to IL-1 beta plus IFN-gamma than normal P cells. Similar results were obtained with beta cells lacking I kappa B kinase beta, a protein kinase required for NF-kappa B activation. Inhibition of P cell NIF-kappa B accelerated the development of autoimmune diabetes in nonobese diabetic mice but had no effect on glucose tolerance or serum insulin in C57BL/6 mice, precluding a nonphysiological effect of transgene expression. Development of diabetes after transfer of diabetogenic CD4(+) T cells was accelerated in RIP-ml kappa B alpha/rionobese diabetic mice and was abrogated by anti-TNF therapy. These results suggest that under conditions that resemble autoimmune type 1 diabetes, the dominant effect of NIF-kappa B is prevention of TNF-induced apoptosis. This differs from the proapoptotic function of NF-kappa B in IL-1 beta-stimulated 6 cells.

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