Stimulation of lymphokines in Jurkat cells persistently infected with vaccinia virus.

Stimulation of lymphokines in Jurkat cells persistently infected with vaccinia virus.
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刺激持续感染牛痘病毒的 Jurkat 细胞中的淋巴因子。

DOI:
10.1128/jvi.66.4.2046-2050.1992
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发表时间:
1992
影响因子:
5.4
通讯作者:
Pogo,BG
Pogo,BG
中科院分区:
医学2区
文献类型:
--
作者:
Stellrecht,KA;Sperber,K;Pogo,BG

文献摘要

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研究了人CD 4 + T细胞系Jurkat对牛痘病毒感染的应答。病毒滴度在感染后约3至4天达到峰值,而细胞生长与未感染细胞的生长相当,表明生长速率不受病毒感染的明显影响。病毒抗原的空斑试验和荧光激活细胞分选仪(FACS)分析的结果表明,建立了持续感染,其中感染细胞的百分比和病毒滴度在传代之间波动。对持续感染的进一步表征表明,病毒影响细胞功能。分别通过酶联免疫吸附测定和FACS分析显示Jvac细胞中白细胞介素-2(IL-2)和IL-2受体α(IL-2 R α)的诱导。细胞RNA与克隆探针的杂交证实了IL-2表达的增加,并证明Jvac细胞也表达更多的IL-6,但不表达γ干扰素(IFN-γ)或IL-1 β。牛痘病毒抗原和IL-2 R α的双抗体染色和FACS分析表明,IL-2 R α的表达仅限于感染的细胞。Jvac细胞对重复感染也有抗性,这是持续感染引起细胞群表型变化的另一个证据。
The response of the human CD4+ T-cell line Jurkat to infection with vaccinia virus was investigated. Virus titers peaked approximately 3 to 4 days after infection, while cell growth paralleled that of uninfected cells, indicating that growth rates were not appreciably affected by viral infection. Results from plaque assays and fluorescence-activated cell sorter (FACS) analyses of virus antigens demonstrated that a persistent infection in which the percentage of infected cells and the virus titers fluctuated from passage to passage was established. Further characterization of the persistent infection revealed that the virus influences cellular functions. Induction of interleukin-2 (IL-2) and IL-2 receptor alpha (IL-2R alpha) in Jvac cells was shown by enzyme-linked immunosorbent assay and FACS analysis, respectively. Hybridization of cellular RNA with cloned probes confirmed the increased IL-2 expression and demonstrated that Jvac cells also expressed more IL-6 but not gamma interferon (IFN-gamma) or IL-1 beta. Dual-antibody staining and FACS analysis for vaccinia virus antigens and IL-2R alpha indicated that IL-2R alpha expression was restricted to the infected cells. Jvac cells were also resistant to superinfection, an additional proof that persistent infection elicited phenotypic changes in the cell population.