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目的探讨NK细胞在TLR9激动剂CpG抑制肝期约氏疟原虫发育中的作用。方法小鼠尾静脉注射NK细胞拮抗剂Anti-Asialo-GM1 40μg后48h给予1 000个约氏疟原虫BY265株子孢子攻击,采用Real-time PCR检测肝脏虫荷并血检疟原虫,分析CpG在NK细胞阻断小鼠中对肝期约氏疟原虫发育的影响。结果 NK细胞阻断后GM1+CpG组小鼠肝脏虫荷与CpG组相比显著增加(t=3.539,P<0.01),与PBS对照组相比显著降低(t=3.658,P<0.01);GM1组与PBS对照组比较差异无统计学意义(t=1.768,P>0.05)。CpG组未出现原虫血症,GM1+CpG组出现原虫血症,但出现时间和PBS对照组相比推迟且原虫血症的峰值降低,小鼠逐渐自愈。PBS组和GM1组小鼠从感染第13d开始出现死亡,第15d全部死亡。结论 NK细胞参与对肝期疟原虫的杀伤过程,TLR9激动剂CpG依赖NK细胞杀伤肝期疟原虫。
Objective To investigate the role of NK cells in inhibiting the development of Plasmodium yoelii during the liver phase by TLR9 agonist CpG. METHODS: One thousand challenged BY265 strains of Plasmodium yoelii were challenged with 40 μg of NK cell antagonist Anti-Asialo-GM1 via tail vein in mice. Real-time PCR was used to detect liver worms and blood samples. CpG Effect of NK cells on the development of Plasmodium yoelii during liver phase in mice. Results Compared with CpG group, the liver burden of GM1 + CpG group was significantly increased (t = 3.539, P <0.01) after NK cells were blocked, which was significantly lower than that of PBS control group (t = 3.658, P <0.01) There was no significant difference between GM1 group and PBS control group (t = 1.768, P> 0.05). The parasitemia did not occur in the CpG group, and parasitemia was observed in the GM1 + CpG group, but the onset time was delayed compared with that in the PBS control group, and the peak value of parasitemia was decreased. The mice gradually self-healed. The mice in the PBS group and the GM1 group died from the 13th day of infection and all died on the 15th day. Conclusion NK cells are involved in the killing process of Plasmodium in the liver stage. The TLR9 agonist CpG relies on NK cells to kill Plasmodium.