NF-kappa B is weakly activated in the NOD mouse model of type 1 diabetes
AuthorIrvin, AE; Jhala, G; Zhao, Y; Blackwell, TS; Krishnamurthy, B; Thomas, HE; Kay, TWH
Source TitleScientific Reports
PublisherNATURE PUBLISHING GROUP
AffiliationMedicine (St Vincent's)
Document TypeJournal Article
CitationsIrvin, A. E., Jhala, G., Zhao, Y., Blackwell, T. S., Krishnamurthy, B., Thomas, H. E. & Kay, T. W. H. (2018). NF-kappa B is weakly activated in the NOD mouse model of type 1 diabetes. SCIENTIFIC REPORTS, 8 (1), https://doi.org/10.1038/s41598-018-22738-3.
Access StatusOpen Access
Type 1 diabetes is an autoimmune disease characterised by selective destruction of pancreatic beta cells by the immune system. The transcription factor nuclear factor-kappa B (NF-κB) regulates innate and adaptive immune responses. Using gene targeting and in vitro analysis of pancreatic islets and immune cells, NF-κB activation has been implicated in type 1 diabetes development. Here we use a non-obese diabetic (NOD) mouse model that expresses a luciferase reporter of transcriptionally active NF-κB to determine its activation in vivo during development of diabetes. Increased luciferase activity was readily detected upon treatment with Toll-like receptor ligands in vitro and in vivo, indicating activation of NF-κB. However, activated NF-κB was detectable at low levels above background in unmanipulated NOD mice, but did not vary with age, despite the progression of inflammatory infiltration in islets over time. NF-κB was highly activated in an accelerated model of type 1 diabetes that requires CD4+ T cells and inflammatory macrophages. These data shed light on the nature of the inflammatory response in the development of type 1 diabetes.
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