NF-κB is weakly activated in the NOD mouse model of type 1 diabetes

11Citations
Citations of this article
21Readers
Mendeley users who have this article in their library.

Abstract

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.

Cite

CITATION STYLE

APA

Irvin, A. E., Jhala, G., Zhao, Y., Blackwell, T. S., Krishnamurthy, B., Thomas, H. E., & Kay, T. W. H. (2018). NF-κB 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

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free