Recombinant murine cytomegalovirus vector activates human monocyte-derived dendritic cells in a NF-κB dependent pathway

被引:11
作者
Wang, Xiuqing [1 ,2 ]
Chen, Ding-geng [3 ,4 ]
机构
[1] S Dakota State Univ, Dept Biol & Microbiol, Brookings, SD 57007 USA
[2] S Dakota State Univ, Ctr Infect Dis Res & Vaccinol, Brookings, SD 57007 USA
[3] S Dakota State Univ, Dept Math & Stat, Brookings, SD 57007 USA
[4] Univ S Dakota, Dept Surg, Sanford Sch Med, Sioux Falls, SD 57105 USA
关键词
Murine cytomegalovirus; Dendritic cells; NF-kappa B; Viral vector; EXPRESSION; APOPTOSIS; RESPONSES;
D O I
10.1016/j.molimm.2009.08.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
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-kappa B) 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-kappa B 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-kappa B dependent pathway. The abortive infection or de novo gene expression greatly enhances the activation of Mo-DC by MCMV vectors. (C) 2009 Elsevier Ltd. All rights reserved.
引用
收藏
页码:3462 / 3465
页数:4
相关论文
共 10 条
[1]
Human cytomegalovirus activates inflammatory cytokine responses via CD14 and toll-like receptor 2 [J].
Compton, T ;
Kurt-Jones, EA ;
Boehme, KW ;
Belko, J ;
Latz, E ;
Golenbock, DT ;
Finberg, RW .
JOURNAL OF VIROLOGY, 2003, 77 (08) :4588-4596
[2]
The murine cytomegalovirus immediate-early 1 protein stimulates NF-kappa B activity by transactivating the NF-kappa B p105/p50 promoter [J].
Gribaudo, G ;
Ravaglia, S ;
Guandalini, L ;
Cavallo, R ;
Gariglio, M ;
Landolfo, S .
VIRUS RESEARCH, 1996, 45 (01) :15-27
[3]
Induction of apoptosis limits cytomegalovirus cross-species infection [J].
Jurak, Igor ;
Brune, Wolfram .
EMBO JOURNAL, 2006, 25 (11) :2634-2642
[4]
The IκB kinase (IKK) and NF-κB:: key elements of proinflammatory signalling [J].
Karin, M ;
Delhase, M .
SEMINARS IN IMMUNOLOGY, 2000, 12 (01) :85-98
[5]
Signal transduction through NF-κB [J].
May, MJ ;
Ghosh, S .
IMMUNOLOGY TODAY, 1998, 19 (02) :80-88
[6]
Recombinant adenovirus induces maturation of dendritic cells via an NF-κB-dependent pathway [J].
Morelli, AE ;
Larregina, AT ;
Ganster, RW ;
Zahorchak, AF ;
Plowey, JM ;
Takayama, T ;
Logar, AJ ;
Robbins, PD ;
Falo, LD ;
Thomson, AW .
JOURNAL OF VIROLOGY, 2000, 74 (20) :9617-9628
[7]
Green fluorescent protein expression in dendritic cells enhances their immunogenicity and elicits specific cytotoxic T-cell responses in humans [J].
Re, F ;
Srinivasan, R ;
Igarashi, T ;
Marincola, F ;
Childs, R .
EXPERIMENTAL HEMATOLOGY, 2004, 32 (02) :210-217
[8]
Identification of a p65 peptide that selectively inhibits NF-κB activation induced by various inflammatory stimuli and its role in down-regulation of NF-κB-mediated gene expression and up-regulation of apoptosis [J].
Takada, Y ;
Singh, S ;
Aggarwal, BB .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (15) :15096-15104
[9]
Mouse cytomegalovirus crosses the species barrier with help from a few human cytomegalovirus proteins [J].
Tang, Qiyi ;
Maul, Gerd G. .
JOURNAL OF VIROLOGY, 2006, 80 (15) :7510-7521
[10]
Murine cytomegalovirus abortively infects human dendritic cells, leading to expression and presentation of virally vectored genes [J].
Wang, XQ ;
Messerle, M ;
Sapinoro, R ;
Santos, K ;
Hocknell, PK ;
Jin, X ;
Dewhurst, S .
JOURNAL OF VIROLOGY, 2003, 77 (13) :7182-7192