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Cell Physiol Biochem. 2018;50(5):1754-1763. doi: 10.1159/000494793. Epub 2018 Nov 1.

Circulating Exosomal miR-17 Inhibits the Induction of Regulatory T Cells via Suppressing TGFBR II Expression in Rheumatoid Arthritis.

Author information

1
Department of Rheumatology and Immunology, Lanzhou University Second Hospital, Lanzhou, China.
2
Department of Rheumatology and Endocrine, Dingxi People's Hospital, Dingxi, China.
3
Department of Cardiology, Lanzhou University Second Hospital, Lanzhou, Chinayujing2304@126.com.

Abstract

BACKGROUND/AIMS:

A reduced prevalence of circulating regulatory T cells (Tregs)is a hallmark of inflammatory rheumatoid arthritis (RA). However, the underlying mechanisms of alterations of Tregs are unclear.

METHODS:

The ratio of Tregs in peripheral blood of healthy controls (HCs) and patients with RA was determined by flow cytometry. MicroRNA (miRNA) expression profiles in exosomes derived from RA patients (RA-exosomes) and in those from HCs (HC-exosomes) were detected by microarray analysis, and miR-17 was measured by quantitative real-time PCR. Transforming growth factor beta receptor II (TGFBR II) expressed by T cells was measured by flow cytometry. The interaction between miR-17 and TGFBR II was evaluated by dual-luciferase reporter assay.

RESULTS:

We found that RA-exosomes can selectively affect Treg differentiation in vitro. Several miRNAs are more abundant in the RA-exosomes than in HC-exosomes. Among those upregulated in patients with RA, miR-17 can suppress Treg induction by inhibiting the expression of TGFBR II.

CONCLUSION:

Our findings imply that altered miRNA expression in RA-exosomes may contribute to the pathogenesis of RA by disrupting the homeostasis of Tregs.

KEYWORDS:

Exosome; Rheumatoid arthritis; TGFBR II; Treg cells; miR-17

PMID:
30384383
DOI:
10.1159/000494793
[Indexed for MEDLINE]
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