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牛病毒性腹泻病毒对单核细胞和树突状细胞的不同作用。

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

作者信息

Glew E J, Carr B V, Brackenbury L S, Hope J C, Charleston B, Howard C J

机构信息

Institute for Animal Health, Compton, Newbury, Berkshire, RG20 7NN UK.

出版信息

J Gen Virol. 2003 Jul;84(Pt 7):1771-1780. doi: 10.1099/vir.0.18964-0.

Abstract

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 non-cytopathic (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.

摘要

多种病原体已被证明可感染抗原呈递细胞,并影响其与T细胞相互作用及刺激T细胞反应的能力。我们使用了一对抗原相同的非细胞病变型(ncp)和细胞病变型(cp)牛病毒性腹泻病毒(BVDV)分离株,以确定这两种生物型如何影响单核细胞和树突状细胞(DC)的功能。我们已经表明,单核细胞和DCs在体外均易受ncp BVDV和cp BVDV感染。此外,感染ncp BVDV的单核细胞刺激同种异体和记忆性CD4(+) T细胞反应的能力受损,但DCs未受影响。这并非由于包括CD80、CD86和CD40在内的多种公认的共刺激分子的下调所致。两种细胞类型对细胞病变病毒感染的反应存在显著差异。树突状细胞对cp BVDV引起的细胞病变效应不敏感,而单核细胞则被杀死。对干扰素(IFN)-α/β产生的分析表明,暴露于cp BVDV的单核细胞和DCs中IFN-α/β水平相似,但暴露于ncp BVDV的细胞中未检测到。我们得出结论,DCs中细胞死亡的预防与IFN-α/β的增强产生无关,如流感病毒的情况,而是通过一种独特的机制。

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