Significance The mechanisms by which autoimmunity is triggered/amplified in T1D remain to be clarified, and the lack of this basic understanding hampers efforts to prevent or arrest the disease. Testing the hypothesis that T1D-associated genetic variants in lncRNAs affect important pathways that modify inflammation and pancreatic β-cell survival will increase our understanding of T1D pathogenesis. In the present paper, we describe a molecular mechanism by which the T1D-associated lncRNA Lnc13 regulates pancreatic β-cell inflammation. These findings provide information on the molecular mechanisms by which disease-associated SNPs in lncRNAs influence disease pathogenesis and open the door for the development of novel diagnostic and therapeutic approaches based on lncRNA targeting.