Division of Allergy, Immunology and Rheumatology, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Dalin 62247, Chiayi, Taiwan.
School of Medicine, Tzu Chi University, Hualien City 97071, Taiwan.
Mediators Inflamm. 2023 Sep 12;2023:2440377. doi: 10.1155/2023/2440377. eCollection 2023.
This study aimed to identify the abnormal expression of long noncoding RNAs (lncRNAs) in T cells from patients with vitiligo and to investigate their functional roles in the immune system. Using microarray analysis, the expression levels of RNA transcripts in T cells from patients with vitiligo and controls were compared. We identified several genes and validated their expression levels in T cells from 41 vitiligo patients and 41 controls. The biological functions of the lncRNAs were studied in a transfection study using an RNA pull-down assay, followed by proteomic analysis and western blotting. The expression levels of 134 genes were significantly increased, and those of 142 genes were significantly decreased in T cells from vitiligo patients. After validation, six genes had increased expression, and three genes had decreased expression in T cells from patients with vitiligo. T-cell expression of LOC100506314 was increased in vitiligo, especially CD4+, but not CD8+ T cells. The expression levels of LOC100506314 in CD4+ T cells was positively and significantly associated with the severity of vitiligo. LOC100506314 was bound to the signal transducer and activator of transcription 3 (STAT3) and macrophage migration inhibitory factor (MIF). Enhanced expression of LOC100506314 inhibited the phosphorylation of STAT3, protein kinase B (AKT), and extracellular signal-regulated protein kinases (ERK), as well as the levels of nuclear protein of p65 and the expression of and in Jurkat cells and T cells from patients with vitiligo. In conclusion, this study showed that the expression of LOC100506314 was elevated in CD4+ T cells from patients with vitiligo and associated the severity of vitiligo. LOC100506314 interacted with STAT3 and MIF and inhibited and expression by suppressing the STAT3, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-B), AKT, and ERK pathways. Enhanced expression of LOC100506314 in T cells may be a potential treatment strategy for vitiligo.
本研究旨在鉴定白癜风患者 T 细胞中长链非编码 RNA（lncRNA）的异常表达，并探讨其在免疫系统中的功能作用。通过微阵列分析，比较了白癜风患者和对照者 T 细胞中的 RNA 转录物表达水平。我们鉴定了几个基因，并在 41 例白癜风患者和 41 例对照者的 T 细胞中验证了其表达水平。通过 RNA 下拉测定、随后进行蛋白质组学分析和 Western blot 进行转染研究，研究了 lncRNA 的生物学功能。在白癜风患者的 T 细胞中，有 134 个基因的表达水平显著升高，有 142 个基因的表达水平显著降低。经验证，6 个基因在白癜风患者的 T 细胞中表达增加，3 个基因在白癜风患者的 T 细胞中表达减少。LOC100506314 在白癜风患者的 T 细胞中表达增加，尤其是 CD4+，但不是 CD8+T 细胞。LOC100506314 在 CD4+T 细胞中的表达水平与白癜风的严重程度呈正相关且显著相关。LOC100506314 与信号转导和转录激活因子 3（STAT3）和巨噬细胞迁移抑制因子（MIF）结合。LOC100506314 的过表达抑制了 Jurkat 细胞和白癜风患者 T 细胞中 STAT3、蛋白激酶 B（AKT）和细胞外信号调节激酶（ERK）的磷酸化以及核蛋白 p65 的水平和 和 的表达。总之，本研究表明，LOC100506314 在白癜风患者的 CD4+T 细胞中表达升高，并与白癜风的严重程度相关。LOC100506314 与 STAT3 和 MIF 相互作用，并通过抑制 STAT3、核因子κB（NF-κB）、AKT 和 ERK 途径抑制 和 的表达。LOC100506314 在 T 细胞中的过表达可能是白癜风的一种潜在治疗策略。
