Link to bioRxiv paper:
http://biorxiv.org/cgi/content/short/2022.12.08.519618v1?rss=1

Authors: Knebel, E., Peleg, S., Dai, C., Cohen-Fultheim, R., Glaser, B., Levanon, E., Powers, A., Klochendler, A., Dor, Y.

Abstract:
A major hypothesis for the etiology of type 1 diabetes (T1D) postulates initiation by viral infection, leading to double-stranded RNA (dsRNA)-mediated interferon response; however, a causal virus has not been identified. Here we use a mouse model, corroborated with human data, to demonstrate that endogenous dsRNA in beta-cells can lead to a diabetogenic immune response, thus identifying a virus-independent mechanism for T1D initiation. We found that disruption of the RNA editing enzyme ADAR in beta-cells triggers a massive interferon response, islet inflammation and beta-cell failure, with features bearing striking similarity to early-stage human T1D. Glycolysis via calcium enhances the interferon response, suggesting an actionable vicious cycle of inflammation and increased beta-cell workload.

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