目的探讨Toll样受体2(Toll-like receptors 2,TLR2)在伯氏疟原虫ANKA株(Plasmodium berghei ANKA,Pb ANKA)诱导的实验脑型疟(experimental cerebral malaria,ECM)中的作用。方法取Pb ANKA采用蚊叮感染、子孢子定量感染和红内期原虫感染3种方式感染TLR2-/-C57BL/6小鼠,同时以WT C57BL/6小鼠为对照。蚊叮感染时,先以Pb ANKA疟原虫感染斯氏按蚊,然后斯氏按蚊通过叮咬实验小鼠使其感染疟原虫。子孢子定量感染时,先以Pb ANKA疟原虫感染斯氏按蚊,然后通过解剖按蚊唾液腺获得疟原虫子孢子,定量注射感染实验小鼠。红内期原虫感染时,先以Pb ANKA疟原虫感染WT C57BL/6小鼠获取感染疟原虫红细胞(parasitized?Red?Blood?Cell,pRBC),然后用pRBC定量感染实验小鼠。通过观测实验小鼠红细胞原虫率、存活率及ECM发生率,判定TLR2是否参与ECM的发生。结果蚊叮感染时,TLR2-/-C57BL/6小鼠与WT C57BL/6小鼠原虫率在ECM发生期间(6~9d)无显著差别,表明TLR2缺失对Pb ANKA疟原虫在小鼠体内的增殖无显著影响。两组小鼠在感染6d后均开始出现偏瘫、昏迷等典型CM症状,9d内全部发生ECM并死亡,ECM发生率均为100%,小鼠存活率均为0。子孢子定量感染时,两组实验小鼠红细胞原虫率无显著差异;小鼠存活率TLR2-/-组为0,WT组为10%;ECM发生率TLR2-/-组为100%,WT组为90%,均无显著差异。红内期原虫感染时,两组实验小鼠红细胞原虫率无显著差异,感染后8d全部发生ECM并死亡,ECM发生率均为100%,小鼠存活率均为0。结论 3种感染实验中小鼠TLR2缺失均未影响ECM的进程,表明ECM的发生不依赖于TLR2的参与。 Objective To investigate the role of Toll-like receptors 2 (TLR2) in experimental cerebral malaria (ECM) induced by Plasmodium berghei ANKA (Pb ANKA). Methods PBR was used to infect TLR2 - / - C57BL / 6 mice with 3 kinds of infection by mosquito binging, quantitative sporozoite infection and protozoal infection by red blood. Meanwhile, WT C57BL / 6 mice were used as control. In the case of mosquito bites, an A. sinensis was first infected with Pb ANKA Plasmodium, which then infected the malaria parasite by bite the experimental mice. Sporozoite quantitative infection, the first to P. ANKA Plasmodium infection Anopheles mosquitoes, and then by dissecting Anopheles salivary glands obtained Plasmodium sporozoites, quantitative injection of experimental mice infected. In the red-stage protozoal infection, parasiticized erythrocytic erythrocytes (pRBC) were infected in WT C57BL / 6 mice with P. aeruginosa Plasmodium, then the experimental mice were quantitatively infected with pRBC. By observing the mouse erythrocytic protozoa rate, survival rate and ECM incidence, to determine whether TLR2 is involved in the occurrence of ECM. Results There was no significant difference in the parasite rate between TLR2 - / - C57BL / 6 mice and WT C57BL / 6 mice during ECM (6-9 days) infection, indicating that TLR2 deletion had no effect on Plasmodium falciparum ANP in mice No significant effect on proliferation. After 6 days of infection, the mice in both groups began to develop typical CM symptoms such as hemiplegia and coma. All of them developed ECM and died within 9 days. The incidence of ECM was 100% and the survival rate of mice was 0. At the time of quantitative sporozoite infection, there was no significant difference in the protozoal rate of erythrocytic between two groups of mice; the survival rate of mice was 0 in TLR2 - / - mice group and 10% in WT group; the incidence of ECM was 100% in TLR2 - / - 90%, no significant difference. During the infection of protozoa in the red stage, there was no significant difference in the number of protozoal cells between the two groups. All the mice died of ECM 8 days after infection, the incidence of ECM was 100% and the survival rate of mice was 0. Conclusion None of the 3 TLR2-deficient mice affected the course of ECM, indicating that the occurrence of ECM does not depend on the involvement of TLR2.