摘要
目的探讨C5a/C5a R信号在约氏疟原虫肝期自然感染和遗传减毒子孢子诱导小鼠保护性免疫中的作用。方法遗传减毒子孢子免疫Balb/c小鼠2、4、6 d后,ELISA检测补体C5a的活化情况;然后利用C5a R-/-Balb/c小鼠,通过定量PCR检测和吉姆萨染色比较子孢子攻击免疫或未免疫2种小鼠的肝脏虫荷和原虫血症。结果子孢子攻击免疫或未免疫的野生与C5a R-/-小鼠的肝脏虫荷和原虫血症之间无统计学差异(P>0.05)。结论遗传减毒子孢子免疫能够成功诱导小鼠产生完全保护性免疫,但补体C5a R缺失对减毒子孢子的免疫保护效果和肝期自然感染均无明显影响,说明C5a/C5a R信号通路并不参与调节约氏疟原虫肝期发育和遗传减毒子孢子诱导小鼠产生的保护性免疫。
To explore the role of C5a/C5 a R signaling in the development of liver-stage Plasmodium and in the protective immunity induced by genetically-attenuated sporozoites（GASs）, Balb/c mice were immunized with GASs and the activation of C5 a was measured by ELISA on 2, 4, 6 days post immunization. Data showed that GASs immunization increased C5 a expression in both WT and C5 a R-/-mice and there was no difference in C5 a expression between them. Furthermore, the Plasmodium burden and the parasitemia were detected by RT-PCR and giemsa＇s staining when GASs-immunized WT and C5 a R-/-mice were challenged with P.yoelii. Giemsa＇s staining showed that GASs could induce the totally-protective immunity against sporozoite in both mice; while PCR results showed that C5 a R deficiency had no impact on the protective immunity induced by GASs and on the natural infection of Plasmodium in liver-stage. All result indicated that C5a/C5 a R signaling does not involve in the process of P. yoelii＇s development in liver-stage or the protective immunity induced by GASs.
出处
《免疫学杂志》
CAS
CSCD
北大核心
2015年第3期221-223,共3页
Immunological Journal
基金
国家自然科学基金面上项目(81271859)
军队自然科学基金(CWS12J093)
关键词
遗传减毒子孢子
免疫
补体
C5A
C5AR
Genetically-attenuated sporozoites
Immunity
Complement
C5a
C5aR
