{"entity": "researcher", "timestamp": "2026-08-25T03:34:10.007Z", "family": "Espinosa", "given": "Alexander", "initials": "A", "orcid": "0000-0003-1107-776X", "affiliations": ["Unit of Rheumatology, Department of Medicine, Karolinska Institutet, Center for Molecular Medicine Karolinska University Hospital, Stockholm, Sweden."], "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/researcher/20b7024111d848c28aca6af51e29d0b2.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/researcher/20b7024111d848c28aca6af51e29d0b2"}}, "publications": [{"entity": "publication", "iuid": "5da4d153f14c4ae79a92b6ae96c5984a", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/5da4d153f14c4ae79a92b6ae96c5984a.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/5da4d153f14c4ae79a92b6ae96c5984a"}}, "title": "miR-31 regulates energy metabolism and is suppressed in T cells from patients with Sj\u00f6gren's syndrome.", "authors": [{"family": "Johansson", "given": "Alina", "initials": "A"}, {"family": "Nyberg", "given": "William A", "initials": "WA"}, {"family": "Sj\u00f6strand", "given": "Maria", "initials": "M"}, {"family": "Moruzzi", "given": "Noah", "initials": "N"}, {"family": "Bergman", "given": "Petra", "initials": "P"}, {"family": "Khademi", "given": "Mohsen", "initials": "M"}, {"family": "Andersson", "given": "Magnus", "initials": "M"}, {"family": "Piehl", "given": "Fredrik", "initials": "F"}, {"family": "Berggren", "given": "Per-Olof", "initials": "PO"}, {"family": "Covacu", "given": "Ruxandra", "initials": "R"}, {"family": "Jagodic", "given": "Maja", "initials": "M"}, {"family": "Espinosa", "given": "Alexander", "initials": "A", "orcid": "0000-0003-1107-776X", "researcher": {"href": "https://publications-affiliated.scilifelab.se/researcher/20b7024111d848c28aca6af51e29d0b2.json"}}], "type": "journal article", "published": "2019-02-00", "journal": {"title": "Eur. J. Immunol.", "issn": "1521-4141", "volume": "49", "issue": "2", "pages": "313-322", "issn-l": "0014-2980"}, "abstract": "Systemic autoimmune diseases are characterized by the overexpression of type I IFN stimulated genes, and accumulating evidence indicate a role for type I IFNs in these diseases. However, the underlying mechanisms for this are still poorly understood. To explore the role of type I IFN regulated miRNAs in systemic autoimmune disease, we characterized cellular expression of miRNAs during both acute and chronic type I IFN responses. We identified a T cell-specific reduction of miR-31-5p levels, both after intramuscular injection of IFN\u03b2 and in patients with Sj\u00f6gren's syndrome (SjS). To interrogate the role of miR-31-51p in T cells we transfected human CD4+ T cells with a miR-31-5p inhibitor and performed metabolic measurements. This identified an increase in basal levels of glucose metabolism after inhibition of miR-31-5p. Furthermore, treatment with IFN-\u03b1 also increased the basal levels of human CD4+ T-cell metabolism. In all, our results suggest that reduced levels of miR-31-5p in T cells of SjS patients support autoimmune T-cell responses during chronic type I IFN exposure.", "doi": "10.1002/eji.201747416", "pmid": "30307034", "labels": [], "xrefs": [], "notes": [], "created": "2026-08-21T11:01:42.799Z", "modified": "2026-08-21T11:01:42.880Z"}]}