Article Summary
党引利,徐 溪,陈丽展,张 瑶,白 丹,吴 朔.干扰素IFNL4对巨噬细胞系THP-1免疫应答的影响[J].现代生物医学进展英文版,2018,(11):2047-2051.
干扰素IFNL4对巨噬细胞系THP-1免疫应答的影响
The Effects of IFNL4 Expression on Immune Response of Macrophages in THP-1 Cell System
Received:November 21, 2017  Revised:December 15, 2017
DOI:10.13241/j.cnki.pmb.2018.11.010
中文关键词: IFNL4  THP-1巨噬细胞  免疫应答  细胞因子  巨噬细胞迁移
英文关键词: IFNL4  THP-1 macrophage  Immune response  Cytokines  Macrophage migration
基金项目:国家自然科学基金项目(81601553)
Author NameAffiliationE-mail
党引利 第四军医大学西京医院呼吸科 陕西 西安 710032 dangyinli1985@163.com 
徐 溪 第四军医大学西京医院呼吸科 陕西 西安 710032  
陈丽展 第四军医大学西京医院呼吸科 陕西 西安 710032  
张 瑶 第四军医大学西京医院呼吸科 陕西 西安 710032  
白 丹 西安交通大学 生物化学与分子生物学系 陕西 西安 710056  
吴 朔 第四军医大学西京医院呼吸科 陕西 西安 710032  
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中文摘要:
      摘要 目的:分析Interferon-lambda 4(IFNL4)表达与巨噬细胞免疫应答间的关系,探讨IFNL4调控免疫应答的信号机制,发掘IFNL4在免疫调理方面的潜在应用价值。方法:建立THP-1细胞培养及分化刺激体系,使用RT-PCR检测不同分化状态THP-1细胞IFNL4的表达水平,并在THP-1细胞中过表达IFNL4,检测IFNL4过表达对THP-1细胞分泌IL-12、TNF-α、IL-10和TGF-β等细胞因子及细胞迁移效率的影响。结果:THP-1细胞分化抑制IFNL4的表达,分化前比分化后IFNL4表达水平相对定量下降255.46倍,差异显著性P<0.001;M2极化巨噬细胞较M1细胞表达IFNL4因子水平升高14.69倍,显著性差异P=0.009;IFNL4过表达可抑制IL-12和TNF-α表达水平,其中TNF-α表达水平变化具有统计学意义(P=0.017),表达水下降5.97倍。IFNL4可促进IL-10和TGF-β的表达,其中TGF-β变化具有统计学意义(P=0.046),表达水平相对上升2.42倍。且IFNL4对THP-1细胞迁移效率具有抑制作用(P=0.005),刺激前细胞迁移数为45.33,IFNL4刺激后迁移数为32.67,迁移移效率下降1.39倍。结论:干扰素IFNL4在分化的M2型THP-1巨噬细胞中具有较高的表达水平,且对THP-1的免疫应答具有一定的抑制作用。
英文摘要:
      ABSTRACT Objective: To investigate the relationship between IFNL4 expression and macrophage functions, analyze the role of IFNL4 in immune regulation, and explore for the potential application value of IFNL4 in immune regulation. Methods: The THP-1 cell culture and stimulation system was esteblished. The IFNL4 expressions in different type of THP-1 cells were detected by RT-PCR. IFNL4 was then overexpressed in THP-1 cells, and the expression of IL-12, TNF-α, IL-10 and TGF-β in these cells were analyzed by RT-PCR. The migration efficiency of THP-1 cells was analyzed by transwell assay before or after IFNL4 overexpression. Results: The differentiation of THP-1 cells inhibited IFNL4 expression (P<0.001), and M2 macrophage can secrete more IFNL4 comparing to M1 macrophage (P=0.009). IFNL4 overexpression in THP-1 cells inhibit IL-12 and TNF-α secretion while promote IL-10 and TGF-β expression, in which TNF-α and TGF-β variations were significantly different (P=0.017 and p=0.046, respectively). Furthermore, IFNL4 overexpression inhibit THP-1 cell migration significantly (P=0.005). Conclusion: IFNL4 has a certain inhibitory effect on inflammation function of macrophage in THP-1 cell system.
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