The location of sensing determines the pancreatic β-cell response to the viral mimetic dsRNAViral infection is an environmental trigger that has been suggested to initiate pancreatic β-cell damage, leading to the development of autoimmune diabetes. Viruses potently activate the immune system and can damage β cells by either directly infecting them or stimulating the production of secondary effector molecules (such as proinflammatory cytokines) during bystander activation. However, how and where β cells recognize viruses is unclear, and the antiviral responses that are initiated following virus recognition are incompletely understood.
Distortion of the Major Histocompatibility Complex Class I Binding Groove to Accommodate an Insulin-derived 10-Mer PeptideBackground CD8+ T-cells play a central role in type 1 diabetes (T1D) by recognizing insulin peptides displayed by MHC. Results A novel flexible MHC binding mode accommodates extra C-terminal peptide residues. Conclusion Unusual peptide-MHC binding might explain weak TCR affinity of a natural T1D epitope. Significance MHC peptide binding can be highly flexible around the F-binding pocket.