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Eur J Immunol. 2019 Feb;49(2):313-322. doi: 10.1002/eji.201747416. Epub 2018 Oct 22.

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

Author information

1
Unit of Rheumatology, Department of Medicine, Karolinska Institutet, Center for Molecular Medicine Karolinska University Hospital, Stockholm, Sweden.
2
The Rolf Luft Research Center for Diabetes and Endocrinology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
3
Unit of Neuroimmunology, Department of Clinical Neuroscience, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
4
Division of Neurology, Karolinska University Hospital, Stockholm, Sweden.

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 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.

KEYWORDS:

Autoimmunity; Immune regulation; Interferons; Metabolism; Rheumatology

PMID:
30307034
DOI:
10.1002/eji.201747416

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