Tat-Rac1 C-末端肽促进树突状细胞的交叉递呈  

Tat-Rac1 C-terminal peptide enhances the cross-presentation of dendritic cells

作　　者：刘婷[1] 邹丽云[1] 万瑛[1] 张晋宇[1] 李娜[1] 李景怡[1] 傅晓岚[1] 吴玉章[1] 

机构地区：[1]第三军医大学全军免疫学研究所,重庆400038

出　　处：《免疫学杂志》2008年第3期283-286,共4页Immunological Journal

摘　　要：目的研究Rac1、Rac2、Rac3、RhoA及Cdc42的C-末端肽对树突状细胞(DC)交叉递呈的影响。方法合成Rac1、Rac2、Rac3、RhoA及Cdc42C末端区与人工改造的穿膜肽Tat47-57的融合肽,负载DC2.4细胞后,采用荧光显微镜及流式细胞术检测DC2.4细胞吞噬能力的变化,采用B3Z细胞检测DC2.4细胞抗原交叉递呈能力的变化。结果负载了Tat-Rac1C-末端肽的DC2.4细胞吞噬能力增强,并显著促进DC2.4细胞经MHCI类分子途径递呈外源性抗原的能力。结论Tat-Rac1C-末端肽能够有效促进DC的交叉递呈,为病毒感染和肿瘤等疾病的治疗奠定了基础。Objective To investigate the function of C-terminal peptides of Rac1, Rac2, Rac3, P, hoA, and Cdc42 on cross-presentation in dendritic cells. Methods ①C-tenninal peptides of Rac1, Rac2, Rac3, RhoA, and Cdc42 were fused with the artificial engineered Tatar_s7 cell-permeable peptide. ②The phagocytosis in DC2.4 cells incubated with the fused peptides was detected by fluorescence microscope and flow cytometry. ③The cross-presentation ability of DC2.4 was measured by B3Z. Results The Tat-Racl C-terminal peptide increased the phagocytosis of DC2.4 cells. And the Tat-Racl C-terminal peptide dramatically enhanced presentation of exogenous antigen on MHC class I molecules in DC2.4 cell. Conclusion The cross-presentation of dendritic cells is effectively enhanced by Tat-Racl C-terminal peptide, which provides a foundation for therapy of virus infection and tumors.

关 键 词：树突状细胞 Rael 交叉递呈 

分 类 号：R392[医药卫生—免疫学]