Abstract:ABSTRACT: Objective This paper discusses the immune regulatory mechanism of the TLR4 agonist - lipopolysaccharide (LPS) in the lethal form of Plasmodium yoelii infection during early stage. Materials and methods 6-8 weeks, female DBA/2 mice were randomly divided into experimental and control groups, intraperitoneally inoculated 1×106 Plasmodium yoelii 17XL(Pyl7XL) parasitized red blood cells. The experimental group was given LPS (25μg/once) intravenously after infection d2. Parasitemia were dynamic observed during the whole infection course. In infected d0, d3, and d5, the number of changes of dendritic cell subsets, dendritic cell surface TLR4, activation of the effect of T cells in the spleen were detected by flow cytometry (FACS). Results (1) the level of parasitemia in LPS treatment mice after infection d5-8 was significantly lower than that in the control group; (2) On d3 and d5 post infection, compared with the control group, LPS treated mouse the number of CD11c+CD11b+DCs and CD11c+CD45R/B220+DCs subsets in the spleen were significantly increased; on d3,CD11c+TLR4+ DCs in the spleen were significantly increased; on d5, CD4+CD69+T lymphocytes in the spleen were significantly increased. Conclusion During the early stage of P.y17XL infection, through the activation of TLR4, LPS can promote the DC maturation and, change its subpopulation proliferation model, and further strengthen the establishment of Th1-type immune response. Then it is obvours obviously decrease the parasitemia. Therefore it will provide new targets for effective antimalarial vaccine development.