畜牧兽医学报 ›› 2014, Vol. 45 ›› Issue (1): 129-135.doi: 10.11843/j.issn.0366-6964.2014.01.018

• 基础兽医 • 上一篇    下一篇

清道夫受体在树突状细胞提呈口蹄疫病毒VP1-VP4抗原中的作用

高云欢,李娜,董昌海,唐然肖,李丽敏,王家鑫*   

  1. (河北农业大学动物医学院免疫学实验室,保定 071000)
  • 收稿日期:2013-07-22 出版日期:2014-01-23 发布日期:2014-01-23
  • 通讯作者: 王家鑫,教授,E-mail: mastwang@163.com
  • 作者简介:高云欢(1988-),男,河北无极人,硕士生,主要从事抗原提呈机制的研究;李娜(1987-),女,河北保定人,硕士生,主要从事抗原提呈机制的研究。二人并列第一作者
  • 基金资助:

    国家自然科学基金资助项目(30972168

The Role of Scavenger Receptors on Dendritic Cells in Presenting VP1-VP4 Antigen of Foot-and-Mouth Disease Virus to T Cells

GAO Yun-huan, LI Na, DONG Chang-hai, TANG Ran-xiao, LI Li-min, WANG Jia-xin*   

  1. (College of Veterinary Medicine, Agricultural University of Hebei, Baoding 071000, China)
  • Received:2013-07-22 Online:2014-01-23 Published:2014-01-23

摘要:

为研究清道夫受体在树突状细胞提呈口蹄疫病毒VP1-VP4融合蛋白中的作用,构建了pET-32a-VP1-VP4原核表达系统,以此获得VP1-VP4融合蛋白。制备骨髓源树突状细胞(BMDCs)和淋巴结T细胞,首先用清道夫受体抑制剂polyI)处理BMDCs,然后再将VP1-VP4融合蛋白负载经polyI)处理后的BMDCs,并与淋巴结T细胞共培养,收集不同时间点的共培养上清液,用ELISA检测其中IFN-γ含量。结果显示,经polyI)处理的试验组在每个时间点产生的IFN-γ含量均明显高于对照组,且差异极显著(P0.01)。表明清道夫受体可识别口蹄疫病毒VP1-VP4融合蛋白,并在BMDCs提呈VP1-VP4抗原的过程中发挥负调节作用。

Abstract:

The aim of this study was to investigate the role of the scavenger receptors on dendritic cells in presentation of recombinant VP1-VP4 of foot-and-mouth disease virus (FMDV) to T cells in vitro. The prokaryotic expression vector of pET-32a-VP1-VP4 was constructed and the VP1-VP4 protein was expressed and purified. Bone marrow-derived dendritic cells (BMDCs) pretreated with scavenger receptor inhibitors were pulsed with recombinant VP1-VP4 antigen and then cocultured with lymph node T cells. The culture supernatants were harvested at different time points for
determining IFN
-γ contents with ELISA. The results showed that the IFN-γ levels of experimental groups were significantly higher than that of control group at different time points (P0.01). Our data indicate that scavenger receptors on BMDCs are able to recognize recombinant VP1-VP4 protein and play a negative regulatory role in antigen presentation of BMDCs to initiate lymph node T cell responses.

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