期刊
CELLULAR & MOLECULAR IMMUNOLOGY
卷 16, 期 3, 页码 260-274出版社
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/cmi.2018.1
关键词
immune dysregulation; mesenchymal stem cells; miR-663; systemic lupus erythematosus; transforming growth factor beta 1
类别
资金
- Major International (Regional) Joint Research Project [81720108020]
- National Natural Science Foundation of China [81373199, 81501347, 81370730, 81273304]
- National Natural Science Foundation of Jiangsu [BK20150098]
- Jiangsu Province Major Research and Development Program [BE2015602]
- Jiangsu Province 333 Talant Grant [BRA2016001]
- Intramural Research Program of NIH, NIDCR
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [ZIADE000101] Funding Source: NIH RePORTER
Mesenchymal stem cells (MSCs) are critical for immune regulation. Although several microRNAs (miRNAs) have been shown to participate in autoimmune pathogenesis by affecting lymphocyte development and function, the roles of miRNAs in MSC dysfunction in autoimmune diseases remain unclear. Here, we show that patients with systemic lupus erythematosus (SLE) display a unique miRNA signature in bone marrow-derived MSCs (BMSCs) compared with normal controls, among which miR-663 is closely associated with SLE disease activity. MiR-663 inhibits the proliferation and migration of BMSCs and impairs BMSC-mediated downregulation of follicular T helper (T-fh) cells and upregulation of regulatory T (T-reg) cells by targeting transforming growth factor beta 1 (TGF-beta 1). MiR-663 overexpression weakens the therapeutic effect of BMSCs, while miR-663 inhibition improves the remission of lupus disease in MRL/lpr mice. Thus, miR-663 is a key mediator of SLE BMSC regulation and may serve as a new therapeutic target for the treatment of lupus.
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