A Role for lncRNAs in Regulating Inflammatory and Autoimmune Responses Underlying Type 1 Diabetes

Type 1 diabetes (T1D) is an autoimmune disease in which immune cells mediate the specific destruction of the insulin-producing β cells in the pancreatic islets. Genetic and transcriptome studies for T1D indicate that a relatively large number of long noncoding RNAs (lncRNAs), detected in both immune cells and β cells, contribute to the underlying inflammation and autoimmune pathology. Although lncRNAs do not encode proteins, their biochemical versatility as RNA molecules enables them to interact with proteins, DNA or RNA to exert regulatory effects on various cellular processes. Recent studies have begun to determine these effects for a small number of lncRNAs in modulating specific immune cell and β-cell responses to elevated glucose levels and pro-inflammatory cytokines that are present within the islets during T1D pathogenesis. These findings are reviewed here and highlight the potential for different lncRNAs to act in concert to inhibit or exacerbate inflammatory and autoimmune responses. Despite this progress to date, additional investigations are required for a more in-depth understanding of their individual functional roles in this interplay, as well as identifying which lncRNAs are likely diagnostic biomarkers or therapeutic targets for autoimmune diseases such as T1D.