Type 1 diabetes (T1D) results from the autoimmune destruction of the pancreatic islets by invading immune cells. Changes in islet gene expression could reveal new insights into this process. The receptor for advanced glycation end products (RAGE), encoded by the AGER gene, is expressed in the islets and immune cells, and AGER polymorphisms affect T1D risk. We analyzed islets from control, non-diabetic autoantibody-positive and T1D donors, to determine if changes in islet gene expression could differentiate these groups when stratified by AGER expression. We found that differences in islet gene expression between autoantibody-positive and T1D donors encompass pathways involved in the activation and regulation of immune cells. Stratification by AGER expression revealed differential expression of FOXP3 among groups. Thus, our findings suggest that changes in AGER may influence islet autoimmunity.

Regulatory T cell genes and pathways associate with islet AGER expression in individuals diagnosed with type 1 diabetes