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Innate immune stimulation of whole blood reveals IFN-1 hyper-responsiveness in type 1 diabetes – published online 05/06/2020

Kameron B. Rodrigues, Matthew J. Dufort, Alba Llibre, Cate Speake, M. Jubayer Rahman, Vincent Bondet, Juan Quiel, Peter S. Linsley, Carla J. Greenbaum, Darragh Duffy, Kristin V. Tarbell

Although type 1 IFN (IFN-1) has been implicated in the early stages of type 1 diabetes pathogenesis, less is known about key innate immune alterations in individuals with established type 1 diabetes. In this issue, Rodrigues, Dufort et al (https://doi.org/10.1007/s00125-020-05179-4)  report findings from their study, which used ex vivo whole blood immune stimulation to show that individuals with type 1 diabetes display higher IFN-1 responses after innate immune stimulation. Furthermore, they show that IFN-γ- and IL-1b-driven responses were not significantly different. Monocytes from NOD mouse models, a strain that develops autoimmune diabetes, also displayed increased IFN-1 responses after treatment with CpG, which stimulates the innate immune system. These findings indicate that increased responsiveness to IFN-1 is a feature of both mouse autoimmune diabetes and human established type 1 diabetes. The authors suggest that a stimulated IFN-1 gene signature could be used as a potential biomarker to identify individuals with type 1 diabetes who may be successfully treated with therapies targeting the IFN-1 pathway.

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