摘要
利用调节性T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,探讨DBA/2小鼠对P.c chabaudi AS感染易感性的原因。DBA/2小鼠对P.c chabaudi AS易感,伴随原虫血症增加CD4+CD25+Foxp3+细胞数量明显增加,且以CD4+CD25+Foxp3hi增加更为明显。原虫血症达峰值时CD4+CD25+Foxp3hi细胞数量亦达到峰值。相比,Treg消除鼠的原虫出现时间和疟血症峰值时间均明显延迟,且在疟血症达峰值前(5～8 d)原虫血症水平明显低于对照组。与之相应,CD4+CD25+Foxp3hi细胞数量明显处于低水平。同时,Treg消除鼠生存期明显延长。由此提示,P.c chabaudi AS感染导致Foxp3表达增加,扩增的CD4+CD25+Foxp3hi细胞有利于疟原虫复制和逃避宿主免疫应答,进而影响疟疾感染的进程和最终结局。
The reason of DBA/2 mice susceptibility to Plasmodium chabaudi chabaudi AS was investigated by using regulatory T cells（Treg） eliminated lethal P.c.chabaudi AS infected mouse malaria model.DBA/2 mice was susceptible to P.c.chabaudi AS followed by the increment of parasitemia with the noticeable increment of CD4^＋CD25^＋Foxp3^＋,especially the increment of CD4^＋CD25^＋Foxp3^hi.When the parasitemia reached to the peak the number of CD4^＋CD25^＋Foxp3^hi cells also reached to the peak.The appearance time of plasmodiaemia in Treg eliminated mice and the appearance time of parasitemia peak was noticeably delayed as compared with control group,and before the parasitemia reached to the peak（5-8 d） the level of plasmodiaemia was noticeably lower than the control group.And the number of CD4^＋CD25^＋Foxp3^hi cells noticeably remained in low level.At the same time,the existing period of Treg eliminated mice were elongated,suggested that P.c.chabaudi AS infection led to the increment of Foxp3 expression thereby.The amplification of CD4^＋CD25^＋Foxp3^hi cells was beneficial to plasmodia to replicate and to escape from the host＇s immune responses,and further affected the course and the final outcomes of malaria infection.
出处
《微生物学杂志》
CAS
CSCD
2012年第2期41-46,共6页
Journal of Microbiology
基金
国家自然科学基金(30800961)
