miR-31 regulates energy metabolism and is suppressed in T cells from patients with Sjögren's syndrome.

Johansson A, Nyberg WA, Sjöstrand M, Moruzzi N, Bergman P, Khademi M, Andersson M, Piehl F, Berggren PO, Covacu R, Jagodic M, Espinosa A

Eur. J. Immunol. 49 (2) 313-322 [2019-02-00; online 2018-10-22]

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 IFNβ and in patients with Sjögren'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-α 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.

PubMed 30307034

DOI 10.1002/eji.201747416

Crossref 10.1002/eji.201747416