Wang Xiuqing, Chen Ding-Geng
Department of Biology and Microbiology, South Dakota State University, Brookings, SD 57007, USA.
Mol Immunol. 2009 Oct;46(16):3462-5. doi: 10.1016/j.molimm.2009.08.001. Epub 2009 Aug 27.
To evaluate the potential use of recombinant murine cytomegalovirus (MCMV) as an antigen delivery vector, we examined the cytokine and CD80 and CD86 expression profiles of MCMV encoding either enhanced green fluorescent protein gene (MCMV-EGFP) or human immunodeficiency virus-1 glycoprotein gp120 gene (MCMV-gp120) infected monocyte-derived dendritic cells (Mo-DC) and investigated the role of nuclear factor kappa B (NF-kappaB) in Mo-DC activation. Results showed that MCMV triggered the induction of inflammatory cytokines and/or CD80 and CD86 up-regulation in Mo-DC. UV-inactivated MCMV exhibited a reduced production of inflammatory cytokines and a lowered expression of CD80 and CD86 compared with live MCMV infection. Treatment of cells with a NF-kappaB peptide inhibitor prior to MCMV infection reduced the induction of cytokines and CD80 and CD86 up-regulation. Overall, the results suggest that recombinant MCMV vectors activate human Mo-DC in a NF-kappaB dependent pathway. The abortive infection or de novo gene expression greatly enhances the activation of Mo-DC by MCMV vectors.
为了评估重组鼠巨细胞病毒（MCMV）作为抗原递送载体的潜在用途，我们检测了编码增强型绿色荧光蛋白基因（MCMV-EGFP）或人类免疫缺陷病毒1型糖蛋白gp120基因（MCMV-gp120）的MCMV感染的单核细胞衍生树突状细胞（Mo-DC）的细胞因子以及CD80和CD86表达谱，并研究了核因子κB（NF-κB）在Mo-DC活化中的作用。结果显示，MCMV可诱导Mo-DC中炎性细胞因子的产生以及CD80和CD86上调。与活MCMV感染相比，紫外线灭活的MCMV诱导炎性细胞因子产生减少，CD80和CD86表达降低。在MCMV感染前用NF-κB肽抑制剂处理细胞可减少细胞因子的诱导以及CD80和CD86上调。总体而言，结果表明重组MCMV载体通过NF-κB依赖途径激活人Mo-DC。流产感染或从头基因表达极大增强了MCMV载体对Mo-DC的活化作用。
