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Patients with autoantibodies to Ro\/SSA (SjD<jats:sup>Ro+<\/jats:sup>) exhibit more severe disease. Long non-coding RNAs (lncRNAs) are a functionally diverse class of non-protein-coding RNAs whose role in autoimmune disease pathology has not been well characterised.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>Whole blood RNA-sequencing (RNA-seq) was performed on SjD cases (n=23 Ro\/SSA negative (SjD<jats:sup>Ro\u2212<\/jats:sup>); n=27 Ro\/SSA positive (SjD<jats:sup>Ro+<\/jats:sup>) and healthy controls (HCs; n=27). Bioinformatics and pathway analyses of differentially expressed (DE) transcripts (log<jats:sub>2<\/jats:sub> fold change \u22652\u2009or \u22640.5; p<jats:sub>adj<\/jats:sub>&lt;0.05) were used to predict lncRNA function. <jats:italic>LINC01871<\/jats:italic> was characterised by RNA-seq analyses of HSB-2 cells with CRISPR-targeted <jats:italic>LINC01871<\/jats:italic> deletion (<jats:italic>LINC01871<jats:sup>\u2212\/<\/jats:sup>\n                     <\/jats:italic>\n                     <jats:sup>\u2212<\/jats:sup>) and in vitro stimulation assays.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>Whole blood RNA-seq revealed autoantibody-specific transcription profiles and disproportionate downregulation of DE transcripts in SjD cases relative to HCs. Sixteen DE lncRNAs exhibited correlated expression with the interferon (IFN)-regulated gene, <jats:italic>RSAD2<\/jats:italic>, in SjD<jats:sup>Ro+<\/jats:sup> (r\u22650.65\u2009or \u2264\u22120.6); four antisense lncRNAs exhibited IFN-regulated expression in immune cell lines. <jats:italic>LINC01871<\/jats:italic> was upregulated in all SjD cases. RNA-seq and pathway analyses of <jats:italic>LINC01871<jats:sup>\u2212\/<\/jats:sup>\n                     <\/jats:italic>\n                     <jats:sup>\u2212<\/jats:sup> cells implicated roles in cytotoxic function, differentiation and IFN\u03b3 induction. <jats:italic>LINC01871<\/jats:italic> was induced by IFN\u03b3 in a myeloid cell line and regulated by calcineurin\/NFAT pathway and T cell receptor (TCR) signalling in primary human T cells.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>\n                     <jats:italic>LINC01871<\/jats:italic> influences expression of many immune cell genes and growth factors, is IFN\u03b3 inducible, and regulated by calcineurin signalling and TCR ligand engagement. Altered <jats:italic>LINC01871<\/jats:italic> expression may influence the dysregulated T cell inflammatory pathways implicated in SjD.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1136\/rmdopen-2022-002672","type":"journal-article","created":{"date-parts":[[2022,12,1]],"date-time":"2022-12-01T13:59:41Z","timestamp":1669903181000},"page":"e002672","update-policy":"https:\/\/doi.org\/10.1136\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":22,"title":["Dysregulated long non-coding RNA in Sj\u00f6gren\u2019s disease impacts both interferon and adaptive immune responses"],"prefix":"10.1136","volume":"8","clinical-trial-number":[{"clinical-trial-number":"nct02327884","registry":"10.18810\/clinical-trials-gov"}],"author":[{"given":"Michelle L","family":"Joachims","sequence":"first","affiliation":[{"name":"Genes and Human Disease Research Program, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA"},{"name":"Arthritis and Clinical Immunology Research 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