Differential effects of bovine viral diarrhoea virus on monocytes and dendritic cells

Differential effects of bovine viral diarrhoea virus on monocytes and dendritic cells
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DOI:
10.1099/vir.0.18964-0
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发表时间:
2003-07-01
影响因子:
3.8
通讯作者:
Howard, CJ
Howard, CJ
中科院分区:
医学3区
文献类型:
--
作者:
Glew, EJ;Carr, BV;Howard, CJ

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各种病原体已被证明可以感染抗原提呈细胞,并影响它们与T细胞反应的相互作用和刺激能力。我们使用了一对抗原性完全相同的非细胞性(NCP)和细胞性(CP)牛病毒性腹泻病毒(BVDV)分离株,以确定这两种生物型对单核细胞和树突状细胞(DC)功能的影响。我们已经证明单核细胞和DC在体外都对NCP BVDV和Cp BVDV敏感。此外,感染NCP BVDV的单核细胞刺激同种异体和记忆性CD4(+)T细胞反应的能力受到损害,但DC没有受到影响。这并不是由于包括CD80、CD86和CD40在内的一些公认的共刺激分子下调所致。这两种细胞类型对感染细胞病变病毒的反应有显著差异。树突状细胞对Cp BVDV引起的细胞病变不敏感,而单核细胞被杀死。干扰素(干扰素)-α/β产生分析显示,在cp BVDV暴露的单核细胞和DC中检测到类似的水平,但在NCP BVDV暴露的细胞中检测不到。我们的结论是,DC中细胞死亡的预防并不像流感病毒所建议的那样与增加干扰素-α/β的产生有关,而是通过一种不同的机制。
Various pathogens have been shown to infect antigen-presenting cells and affect their capacity to interact with and stimulate T-cell responses. We have used an antigenically identical pair of noncytopathic (ncp) and cytopathic (cp) bovine viral diarrhoea virus (BVDV) isolates to determine how the two biotypes affect monocyte and dendritic cell (DC) function. We have shown that monocytes and DCs are both susceptible to infection with ncp BVDV and cp BVDV in vitro. In addition, monocytes infected with ncp BVDV were compromised in their ability to stimulate allogeneic and memory CD4(+) T cell responses, but DCs were not affected. This was not due to down-regulation of a number of recognized co-stimulatory molecules including CD80, CD86 and CD40. Striking differences in the response of the two cell types to infection with cytopathic virus were seen. Dendritic cells were not susceptible to the cytopathic effect caused by cp BVDV, whereas monocytes were killed. Analysis of interferon (IFN)-alpha/beta production showed similar levels in monocytes and DCs exposed to cp BVDV, but none was detected in cells exposed to ncp BVDV. We conclude that the prevention of cell death in DCs is not associated with enhanced production of IFN-alpha/beta, as proposed for influenza virus, but is by a distinct mechanism.