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PharMolix KG

IFN receptor

Type 1
diabetes

IFNα upregulates HLA-I, cytokines, chemokines, and causes ER stress in pancreatic islets. Targeting IFNα represents a potential therapeutic strategy in the early stages of T1D.

The pathogenesis of human type 1 diabetes, characterized by immune-mediated damage of insulin-producing b-cells of pancreatic islets, may involve viral infection. Essential components of the immune antiviral response, including type I interferon (IFN) and IFN receptor-mediated signaling pathways, are candidates for determining susceptibility to human type 1 diabetes.

A diminished IFN-gamma secretion and the association of fasting C-peptide levels with cytokine response in children with type 1 diabetes suggest that factors related to beta-cell function in type 1 diabetes may modify T-cell function. Thus, the T-cell responses detected at or after diagnosis may not reflect the pathogenic process leading to type 1 diabetes.