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Clin Immunol. 2014 Jan;150(1):22-30. doi: 10.1016/j.clim.2013.10.009. Epub 2013 Oct 25.

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

Author information

1
Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, 410011 Hunan, China.
2
Division of Allergy, Asthma and Immunology, Department of Pediatrics, Thomas Jefferson University Hospital, USA.
3
Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, 410011 Hunan, China. Electronic address: suyuwen@medmail.com.cn.
4
Department of Dermatology, Second Xiangya Hospital, Central South University, Hunan Key Laboratory of Medical Epigenomics, Changsha, 410011 Hunan, China. Electronic address: qianlu5860@gmail.com.

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.

KEYWORDS:

CD4(+) T cells; FOXP3; MicroRNA; Psoriasis vulgaris; Treg cells; miR-210

PMID:
24316592
DOI:
10.1016/j.clim.2013.10.009
[Indexed for MEDLINE]
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