miR-31 regulates energy metabolism and is suppressed in Tcells from patients with Sjögren's syndrome

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 miRNA...

Full description

Saved in:
Bibliographic Details
Published in:European journal of immunology 2019, Vol.49 (2), p.313
Main Authors: Johansson, Alina, Nyberg, William A., Sjostrand, Maria, Moruzzi, Noah, Bergman, Petra, Khademi, Mohsen, Andersson, Magnus, Piehl, Fredrik, Berggren, Per-Olof, Covacu, Ruxandra, Jagodic, Maja, Espinosa, Alexander
Format: Article
Language:English
Subjects:
Autoimmunity
Immune regulation
Interferons
Metabolism
Rheumatology
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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 Tcell-specific reduction of miR-31-5p levels, both after intramuscular injection of IFN and in patients with Sjogren's syndrome (SjS). To interrogate the role of miR-31-51p in Tcells we transfected human CD4(+) Tcells 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- also increased the basal levels of human CD4(+) T-cell metabolism. In all, our results suggest that reduced levels of miR-31-5p in Tcells of SjS patients support autoimmune T-cell responses during chronic type I IFN exposure.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.201747416