Up-regulation of microRNA-210 induces immune dysfunction via targeting FOXP3 in CD4+ T cells of psoriasis vulgaris

Abstract Psoriasis vulgaris (PV) is a chronic inflammatory and T cell-mediated autoimmune skin disease. An immune dysfunction that is manifested by abnormally activated T cells and defective regulatory T (Treg) cells may play an important role in the pathogenesis of PV. However, the precise mechanis...

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Bibliographic Details
Published in:Clinical immunology (Orlando, Fla.) Fla.), 2014-01, Vol.150 (1), p.22-30
Main Authors: Zhao, Ming, Wang, Li-tao, Liang, Gong-ping, Zhang, Peng, Deng, Xin-jie, Tang, Qian, Zhai, Han-yue, Chang, Christopher C, Su, Yu-wen, Lu, Qian-jin
Format: Article
Language:English
Subjects:
Adult
Allergy and Immunology
CD4+ T cells
CD4-Positive T-Lymphocytes - immunology
Cytokines - genetics
Female
Forkhead Transcription Factors - genetics
Forkhead Transcription Factors - immunology
FOXP3
Humans
Male
MicroRNA
MicroRNAs - biosynthesis
MicroRNAs - genetics
Middle Aged
miR-210
Psoriasis - genetics
Psoriasis - immunology
Psoriasis vulgaris
RNA, Messenger - biosynthesis
Treg cells
Up-Regulation
Young Adult
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Summary:Abstract Psoriasis vulgaris (PV) is a chronic inflammatory and T cell-mediated autoimmune skin disease. An immune dysfunction that is manifested by abnormally activated T cells and defective regulatory T (Treg) cells may play an important role in the pathogenesis of PV. However, the precise mechanism of the immune dysfunction in PV patients still remains unclear. In this study, we found that miR-210 expression is increased significantly in CD4+ T cells from patients with PV and confirmed that FOXP3 is a target gene of miR-210. We also found that overexpression of miR-210 inhibits FOXP3 expression and impairs the immunosuppressive functions of Treg cells in CD4+ T cells from healthy controls. In contrast, inhibition of miR-210 increases FOXP3 expression and reverses the immune dysfunction in CD4+ T cells from patients with PV. Our data demonstrates that increased miR-210 induces immune dysfunction via by FOXP3 in CD4+ T cells from patients with PV.
ISSN:1521-6616
1521-7035
DOI:10.1016/j.clim.2013.10.009