[目的 ]观察预感染巴西日圆线虫后 ,小鼠抵御伯氏疟原虫攻击感染的能力 ,并着重探讨T辅助细胞亚型在感染过程中的变化以及这些变化对宿主免疫力和预后的影响。 [方法 ]皮下注射巴西日圆线虫感染C5 7BL/ 6小鼠 ,建立线虫预感染模型 ,于 3wk后腹腔注射伯氏疟原虫ANKA株攻击感染小鼠。观察每天原虫血症变化情况 ,并于疟原虫感染后 0、3和 9d取脾 ,提取RNA ,用RT PCR扩增法定性观察细胞因子IFN γ和IL 4的变化。[结果 ]与对照组相比 ,实验组感染疟原虫后 ,原虫血症的峰值出现时间明显延长 ,小鼠对疟原虫感染的耐受程度以及小鼠生存时间显著提高。实验组Th2型细胞合成IL 4的量在疟原虫感染 0d时明显高于对照组 ;而在 3与 9d时两组均异常升高。Th1型细胞合成IFN γ的量在疟原虫感染后 3d时实验组高于对照组 ,但在 9d时实验组IFN γ有所下降。 [结论 ]预感染巴西日圆线虫的小鼠具有较高的抗感染能力。但在攻击感染疟原虫后Th2型细胞被提前激活而抑制了Th1型细胞的正常功能 ,最终仍导致小鼠死亡。 [Objective] The purpose of this study was to observe the ability of mice to resist infection with Plasmodium berghei after pre-infection with C. elegans and to investigate the changes of T-helper cell subtypes during infection and the effects of these changes on host immunity and prognosis. [Method] C5 7BL / 6 mice were inoculated subcutaneously with C. elegans to establish a nematode pre-infection model. The infected mice were challenged with ANKA strain of Plasmodium berghei intraperitoneally after 3 weeks. The changes of protozoa were observed daily. The spleens were harvested at 0, 3 and 9 days after infection with Plasmodium, RNA was extracted and the changes of cytokine IFN-γ and IL-4 were observed by RT-PCR. [Result] Compared with the control group, the peak time of parasitemia was significantly prolonged in the experimental group infected with malaria parasite, and the tolerance of the mice to the parasite infection and the survival time of the mice were significantly increased. The amount of IL-4 synthesized by Th2 cells in experiment group was significantly higher than that of control group on the 0d of Plasmodium infection, but was abnormally increased in both groups at 3 and 9 days. The amount of IFNγ synthesized by Th1 cells in the experimental group was higher than that in the control group at 3d after the infection of Plasmodium, but IFNγ in the experimental group decreased at 9d. [Conclusion] The mice pre-infected with C. elegans had higher anti-infective capacity. However, Th2 cells were activated in advance after challenge with Plasmodium infection, inhibiting the normal function of Th1 cells and eventually leading to the death of mice.