Regulation of CD4+ CD25+ Foxp3+ regulatory T cells ( Treg cells) on Th2 polarization during malaria infection was investigated. Plasmodium chabaudi chabaudi AS obliterated by Tregs cells was used to infect mice malaria model to carry out the study. The results showed that the peak of plasmodiaemia was as high as 40. 5% 8 days after the infection, then inclined rapidly in subsequence and self-recovered 18 days after the infection. As comparison, 10 days after the infection, the plasmodiaemia of the Treg cells obliterated group rapidly rose to 32% , and the mice died successively in the subsequence. 8 ~10 days after the infection the mice with Treg obliteration, the percentage content of their spleen CD4+ CD25+ Foxp3+ accounted in CD4+ was significantly lower than the control group. At the same time, the level of both serum plasmodial specific antibody IgGl and IgG2a was obviously declined. The results suggested that during P. C. Chabaudi AS infection CD4+ CD25+ Foxp3+ took part in the polarization of regulatory Th2 cell immune responses, and moreover meddled with the plasmodia to obliterate.%为探讨CD4+ CD25+ Foxp3+调节性T细胞(Treg细胞)在疟疾感染过程中对Th2极化的调控作用,利用Treg细胞消除的致死型夏氏疟原虫(Plasmodium chabaudi chabaudi AS,P.c chabaudi AS)感染鼠疟模型进行研究.结果显示,对照组小鼠在感染后8d原虫血症达到峰值40.5％,随后迅速下降,于感染后18 d小鼠自愈.相比,Treg细胞消除组于感染后10d,原虫血症水平迅速上升至32％,随后小鼠相继死亡.在感染后8～10 d,Treg细胞消除小鼠脾脏CD4+ CD25+ Foxp3+细胞占CD4+细胞百分比含量明显低于对照组.同时,血清疟原虫特异性抗体IgG1和IgG2a水平均明显降低.结果提示,P.cchabaudi AS感染中CI4+ CD25+ Foxp3+细胞参与调控Th2型免疫应答的极化,进而干预疟原虫清除.
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