So Young Na1, Mi-Jin Park1, Sun Park2, Eun-So Lee3. 1. Department of Dermatology, Ajou University School of Medicine, Suwon, South Korea. 2. Department of Microbiology, Ajou University School of Medicine, Suwon, South Korea. 3. Department of Dermatology, Ajou University School of Medicine, Suwon, South Korea. esl@ajou.ac.kr.
Abstract
OBJECTIVES: The goal of this study was to investigate whether microRNA-155 might be a potential therapeutic target for Behçet's disease (BD). METHODS: Expression levels of miR-155 were quantified using TaqMan microRNA assays in peripheral blood mononuclear cells and in isolated CD4+ T cells from BD patients and healthy controls. To identify targets of miR-155, luciferase reporter assays and western blotting were performed. The effect of miR-155 on Th17 polarisation was analysed in patients with active BD by using flow cytometry and enzyme-linked immunosorbent assay. RESULTS: The expression of miR-155 and IL-17 was significantly increased in CD4+ T cells of patients with active BD. A luciferase reporter assay and western blot showed that Ets-1 expression was reduced by miR-155 mimics. Furthermore, the expression of Ets-1 was significantly decreased in patients with active BD compared to healthy controls. More importantly, repression of miR-155 in CD4+ T cells from active BD patients increased Ets-1 expression and reduced the number of IL- 17-expressing T cells and overall IL-17 production. CONCLUSIONS: MiR-155 regulates the Th17 immune response by targeting Ets-1. Suppression of miR-155 reduced the amount of pathogenic IL-17-expressing T cells and may be a potential therapeutic strategy for BD.
OBJECTIVES: The goal of this study was to investigate whether microRNA-155 might be a potential therapeutic target for Behçet's disease (BD). METHODS: Expression levels of miR-155 were quantified using TaqMan microRNA assays in peripheral blood mononuclear cells and in isolated CD4+ T cells from BD patients and healthy controls. To identify targets of miR-155, luciferase reporter assays and western blotting were performed. The effect of miR-155 on Th17 polarisation was analysed in patients with active BD by using flow cytometry and enzyme-linked immunosorbent assay. RESULTS: The expression of miR-155 and IL-17 was significantly increased in CD4+ T cells of patients with active BD. A luciferase reporter assay and western blot showed that Ets-1 expression was reduced by miR-155 mimics. Furthermore, the expression of Ets-1 was significantly decreased in patients with active BD compared to healthy controls. More importantly, repression of miR-155 in CD4+ T cells from active BD patients increased Ets-1 expression and reduced the number of IL- 17-expressing T cells and overall IL-17 production. CONCLUSIONS:MiR-155 regulates the Th17 immune response by targeting Ets-1. Suppression of miR-155 reduced the amount of pathogenic IL-17-expressing T cells and may be a potential therapeutic strategy for BD.
Authors: Sally S Hassouna; Manal Y Tayel; Ashraf I Alzawawy; Dalal M Elkaffash; Ahmed M Abdel Hadi; Eman H Elsayed; Rowayda M Amin; Eman Tayae; Alya Elkayal; Asmaa Nasr Journal: Mediterr J Rheumatol Date: 2020-09-30
Authors: Xin Yu; Meifang Wang; Linfeng Li; Lin Zhang; Matthew Tak Vai Chan; William Ka Kei Wu Journal: J Cell Mol Med Date: 2020-04-30 Impact factor: 5.310