基础医学与临床 ›› 2015, Vol. 35 ›› Issue (12): 1640-1644.

• 研究论文 • 上一篇    下一篇

抗中性粒细胞胞浆抗体诱导FcγRIIa升高与血管炎相关细胞因子的关系

何建业1,魏丹丹2,林旭红2,白春洋2   

  1. 1. 开封市儿童医院
    2. 河南大学淮河医院
  • 收稿日期:2015-06-01 修回日期:2015-10-09 出版日期:2015-12-05 发布日期:2015-12-04
  • 通讯作者: 白春洋 E-mail:13937855282@126.com
  • 基金资助:
    Fcγ受体阻断剂治疗ANCA相关性血管炎的分子机制研究

Expression of FcγRⅡa induced by Antineutrophil cytoplasmic antibody is related with cytokines

  • Received:2015-06-01 Revised:2015-10-09 Online:2015-12-05 Published:2015-12-04

摘要: 目的 探讨抗中性粒细胞胞浆抗体通过影响中性粒细胞膜上FcγRⅡa的表达参与疾病进程。方法 用不同浓度的抗中性粒细胞胞浆抗体相关血管炎活动期血清,分别是抗髓过氧化物酶抗体及抗蛋白酶3抗体阳性血清刺激健康人中性粒细胞,以健康人血清刺激中性粒细胞作为对照组,用流式细胞术分析血液中FcγRIIa的荧光强度,Western blot分析FcγRIIa的表达,鲁米诺化学发光方法检测中性粒细胞中氧自由基生成,用酶联免疫吸附试验检测血清细胞因子TNF-α、IL-6的水平及血清中抗髓过氧化物酶抗体及抗蛋白酶3抗体水平。结果 伴随血清浓度的降低,FcγRⅡa 荧光强度、FcγRIIa蛋白的表达、中性粒细胞中氧自由基及其分泌的细胞因子TNF-α、IL-6水平下降(P<0.05)。结论 抗髓过氧化物酶抗体及抗蛋白酶3抗体可能均通过FcγRIIa影响氧自由基生成及细胞因子TNF-α、IL-6的水平,进而导致血管炎的发生。

关键词: ANCA相关性血管炎, Fcγ受体IIa, 细胞因子

Abstract: Objective To investigate antineutrophil cytoplasmic antibody resulting in antineutrophil cytoplasmic antibody-associated vasculitides by influencing the expression of FcγRⅡa in the cell membrane. Methods Human neutrophils were stimulated by different concentration serum (anti-myeloperoxidase antibody positive and anti-proteinase 3 positive), healthy human serum as control. Flow cytometry was used to detect the expression of FcγRIIa in the neutrophil membrane. FcγRIIa were analyzed by Western blots. Reactive oxygen species(ROS) production was measured by chemiluminescence technique in the presence of 10 mM luminol. Enzyme linked immunosorbent assay (ELISA) was applied to detect the level of serum cytokines TNF-α, IL-6, anti-myeloperoxidase antibody and anti-proteinase 3. Results With the decrease of serum concentration, fluorescence intensity of FcγRIIa expression, the expression of FcγRIIa, ROS generation and secretion of cytokines TNF-α and IL-6 reduced(P<0.05). Conclusion Anti-myeloperoxidase antibody and anti-proteinase 3 antibody maybe play a role in mediating ROS, TNF-α and IL-6 levels through FcγRIIa, and induce the generation of antineutrophil cytoplasmic antibody associated vasculitis.

Key words: ANCA associated vasculitis, Fc gamma receptor IIa, Cytokines