期刊
EXPERIMENTAL DERMATOLOGY
卷 29, 期 7, 页码 623-629出版社
WILEY
DOI: 10.1111/exd.14111
关键词
biomarker; immunosuppression; miRNA; pemphigus vulgaris; regulatory T cell
类别
资金
- National Natural Science Foundation of China [81673067]
- Guangdong Science and Technology Plan Project [2016A020215116]
Pemphigus vulgaris (PV) is a regulatory T cell (Treg)-associated autoimmune disease. Treg cells maintain immunosuppression by expressing the signature transcription factor FOXP3. MicroRNAs (miRNAs) have frequently emerged as regulators in Treg-mediated immunosuppression. We previously found that miR-338-3p was overexpressed in the peripheral blood mononuclear cells of patients with PV. Herein, we explored the role of miR-338-3p in Treg-mediated immunosuppression by quantitative real-time polymerase chain reaction, analysis of public microarray data, miRNA transfection, Western blotting, flow cytometry, and luciferase reporter assays. Increased expression of miR-338-3p was detected in CD4+ T cells of active PV patients compared with those in healthy controls. Moreover, the miR-338-3p level was positively related to disease severity. Bioinformatics prediction revealed that Runt-related transcription factor 1 (RUNX1), a gene activatingFOXP3expression, was a putative target of miR-338-3p. There was a reduction ofFOXP3andRUNX1 expression in the CD4+ T cells of patients with PV, along with significant correlations with the level of miR-338-3p. MiRNA transfection, mRNA and protein analysis, and luciferase reporter assays verified that miR-338-3p attenuatedFOXP3expression by targetingRUNX1. This study suggests that excessive expression of miR-338-3p attenuates the expression ofFOXP3 by targetingRUNX1, contributing to Treg dysfunction in PV.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据