CAJ | 학술논문

目的探讨致死型约氏疟原虫(Plasmodium yoelii 17XL,P.y17XL)感染早期,Toll样受体(Toll like receptor,TLR)在树突状细胞(dendritic cells, DCs)活化中的作用地位.方法用P.y 17XL感染易感的BALB/c和抵抗的DBA/2小鼠,计数红细胞感染率;制备感染前和感染后第3d、5d小鼠脾细胞悬液,采用流式细胞分析技术检测两种小鼠感染不同时间脾细胞悬液中细胞内表达TLR9(Toll like receptor 9,TLR9)的DCs和细胞表面表达TLR4(Toll like receptor 4,TLR4)的DCs的百分含量.结果两种小鼠脾DCs细胞内TLR9的表达水平均于感染后第3d开始明显升高(P<0.01),在第5d达到最高水平(P<0.01),但两种小鼠相比无统计学意义.同时,两种小鼠DCs表面TLR4的表达水平均未见明显变化.结论在P.y 17XL感染早期,TLR9可能是介导DCs活化的模式识别受体.
목적 탐토치사형약씨학원충(Plasmodium yoelii 17XL,P.y17XL)감염조기,Toll양수체(Toll like receptor,TLR)재수돌상세포(dendritic cells, DCs)활화중적작용지위.방법 용P.y 17XL감염역감적BALB/c화저항적DBA/2소서,계수홍세포감염솔;제비감염전화감염후제3d、5d소서비세포현액,채용류식세포분석기술검측량충소서감염불동시간비세포현액중세포내표체TLR9(Toll like receptor 9,TLR9)적DCs화세포표면표체TLR4(Toll like receptor 4,TLR4)적DCs적백분함량.결과 량충소서비DCs세포내TLR9적표체수평균우감염후제3d개시명현승고(P<0.01),재제5d체도최고수평(P<0.01),단량충소서상비무통계학의의.동시,량충소서DCs표면TLR4적표체수평균미견명현변화.결론 재P.y 17XL감염조기,TLR9가능시개도DCs활화적모식식별수체.
To investigate the role of Toll like receptor (TLR) in the activation of dendritic cells (DC) during early Plasmodium yoelii infection of the lethal strain 17XL (P.y 17XL), susceptible BALB/c and resistant DBA/2 mice were infected by i.p.injection of the P.y l7XL-parasitized erythrocytes, and the parasitemia of individua1 mice was monitored by the microscopic examination of blood smear stained with Giemsa.Mice from norma1 and infected groups were sacrificed on 0,3 and 5 days post-infection to collect their spleen cells.And the expressions of TLR-9 and TLR-4 on the cell surface of DCs in spenonocytes of these two strains of mice were assayed by applying flow cytometry to quantitatively analyze the percentages of CD11c+TLR9+ DCs and CD11c+TLR4+ DCs. It was found that the population of CD11c+DCs expressing TLR9 was significantly increased on day 3 and peaked on 5 p.i. in BALB/c (P<0.01) and DBA/2 mice(P<0.01). However, there was no statistical significance between these two strains of mice. Meanwhile, there was no change on the population of CD11c+ DCs expressing TLR4 in BALB/c and DBA/2 mice. These results indicate that TLR9 may contribute to the DC activation during early stages of P.y17XL infection.