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Most T1D\u2010associated single nucleotide polymorphisms (SNPs) are located in non\u2010coding regions of the human genome. Interestingly, SNPs in long non\u2010coding RNAs (lncRNAs) may result in the disruption of their secondary structure, affecting their function, and in turn, the expression of potentially pathogenic pathways. In the present work, the function of a virus\u2010induced T1D\u2010associated lncRNA named\n                    <jats:italic>ARGI<\/jats:italic>\n                    (Antiviral Response Gene Inducer) is characterized. Upon a viral insult,\n                    <jats:italic>ARGI<\/jats:italic>\n                    is upregulated in the nuclei of pancreatic\n                    <jats:italic>\u03b2<\/jats:italic>\n                    cells and binds to CTCF to interact with the promoter and enhancer regions of IFN\n                    <jats:italic>\u03b2<\/jats:italic>\n                    and interferon\u2010stimulated genes, promoting their transcriptional activation in an allele\u2010specific manner. The presence of the T1D risk allele in\n                    <jats:italic>ARGI<\/jats:italic>\n                    induces a change in its secondary structure. Interestingly, the T1D risk genotype induces hyperactivation of type I IFN response in pancreatic\n                    <jats:italic>\u03b2<\/jats:italic>\n                    cells, an expression signature that is present in the pancreas of T1D patients. These data shed light on the molecular mechanisms by which T1D\u2010related SNPs in lncRNAs influence pathogenesis at the pancreatic\n                    <jats:italic>\u03b2<\/jats:italic>\n                    cell level and opens the door for the development of therapeutic strategies based on lncRNA modulation to delay or avoid pancreatic\n                    <jats:italic>\u03b2<\/jats:italic>\n                    cell inflammation in T1D.\n                  <\/jats:p>","DOI":"10.1002\/advs.202300063","type":"journal-article","created":{"date-parts":[[2023,6,29]],"date-time":"2023-06-29T06:30:20Z","timestamp":1688020220000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["LncRNA\n                    <i>ARGI<\/i>\n                    Contributes to Virus\u2010Induced Pancreatic\n                    <i>\u03b2<\/i>\n                    Cell Inflammation Through Transcriptional Activation of IFN\u2010Stimulated Genes"],"prefix":"10.1002","volume":"10","author":[{"given":"Itziar","family":"Gonz\u00e1lez\u2010Moro","sequence":"first","affiliation":[{"name":"Department of Biochemistry and Molecular Biology University of the Basque Country  Leioa 48940 Spain"},{"name":"Biocruces Bizkaia Health Research Institute  Barakaldo 48903 Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Koldo","family":"Garcia\u2010Etxebarria","sequence":"additional","affiliation":[{"name":"Biodonostia Health Research Institute Gastrointestinal Genetics Group  San Sebasti\u00e1n 20014 Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Enfermedades Hep\u00e1ticas y Digestivas (CIBERehd)  Barcelona 08036 Spain"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Luis Manuel","family":"Mendoza","sequence":"additional","affiliation":[{"name":"Department of Biochemistry and Molecular Biology University of the Basque Country  Leioa 48940 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