伯氏疟原虫感染早期的根治性治疗对再感染体液免疫应答的影响

为探讨疟疾感染早期根治性治疗对再感染体液免疫应答的影响,用伯氏疟原虫感染DBA/2小鼠,感染后3天进行根治性治疗,并于初次感染后90天再进行感染.通过薄血膜吉姆萨染色法计数红细胞感染率,流式细胞术检测再感染前(0天)和再感染后(1、3、5天)不同时间点脾细胞中活化性B细胞百分率,ELISA检测血清中特异性IgG、IgG...

Effect of radical treatment in early phase of primary infection with P.berghei ANKA on humoral immune response to homologous reinfection

To investigate the effect of radical treatment in early phase of primary infection with Plasmodium spp. on humoral immune response to homologous reinfection, DBA/2 mice were infected by intraperitoueal injection of 1 × l06 P. berghei ANKA parasited erythrocytes, and radically treated with chloroquine plus artesunate on day 3 after infection. The mice were reinfected with P. berghei ANKA on day 90 after primary infection. The level of parasitemia during primary and secondary infection was observed by means of the Giemsa staining of thin blood smears, and applying flow eytometry to quantitively analyze the percentage of activated B cells in spleen cell population at day 0, 1, 3 and 5 post-reinfection, respectively, the levels of specific IgG and its subclasses IgG1, IgG2a as well as IgE Abs in sera were also measured by ELISA at the same time. It was found that, after reinfection, parasitemia in radically treated mice was transient and extremely low, and that percentage of activated B cells in these mice began increase on day 3 post-reinfection, also, their levels of specific lgG and its subclasses IgG1, IgG2a simultaneously began to increase, moreover, the levels of IgG, IgG1 and IgG2a from radically treated mice were higher than that in normal mice （non-infected） before reinfection, and IgG2a were always higher than IgG1 at each time point, IgE showed a significant increase on day 1 post-reinfection. These results suggested that radical treatment in early phase of primary infection with Plasmodium spp. took less effect on humoral immune response to homologous reinfection. The persistence of some memory B cells and long-lived plasma ceils might be important for the host against homologous reinfection, specific lgG, particularly its subclasses IgG2a, and might be the key factor involved in protective immunity against homologous reinfection.