IL-2 independent growth and cytotoxicity of herpesvirus saimiri-infected human CD8 cells and involvement of two open reading frame sequences of the virus.

IL-2 independent growth and cytotoxicity of herpesvirus saimiri-infected human CD8 cells and involvement of two open reading frame sequences of the virus.
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疱疹病毒 saimiri 感染的人 CD8 细胞的 IL-2 独立生长和细胞毒性以及病毒的两个开放阅读框序列的参与。

DOI:
10.1006/viro.1993.1495
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发表时间:
1993
期刊:
影响因子:
3.7
通讯作者:
Medveczky,PG
Medveczky,PG
中科院分区:
医学3区
文献类型:
--
作者:
Medveczky,MM;Geck,P;Sullivan,JL;Serbousek,D;Djeu,JY;Medveczky,PG

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赛米尔疱疹病毒是一种灵长类肿瘤病毒,可在新世界猴和兔子中诱导急性 T 细胞淋巴瘤和白血病。我们在这份报告中表明,用 C 组菌株 484-77 感染人外周血白细胞会导致具有强细胞毒活性的 CD8 淋巴细胞选择性扩增,并且这些细胞不需要白细胞介素 2 (IL-2) 来生长。受感染的细胞培养物,称为疱疹病毒激活杀伤 (HAK) 细胞,已在组织培养物中连续维持数月,这些 HAK 细胞含有多个稳定的环状病毒附加体副本。发现 HAK 细胞的生长和细胞毒性不依赖于 IL-2。对缺失突变体感染细胞的分析表明,病毒基因组编码的双顺反子 mRNA 的至少两个开放阅读框序列参与控制 IL-2 独立性。该模型可以促进对人类细胞毒性 T 细胞生长调节的研究,这些细胞是针对传染病和癌症的免疫反应中的重要效应细胞,并应帮助我们阐明幽门螺旋杆菌的转化机制。 Saimirioncogenes。
Herpesvirus saimiriis a primate tumor virus and induces acute T cell lymphomas and leukemias in New World monkeys and rabbits. We show in this report that infection of human peripheral white blood cells with a group C strain 484-77 results in selective expansion of CD8 lymphocytes with strong cytotoxic activity and these cells do not require interleukin-2 (IL-2) for growth. Infected cell cultures, termed herpesvirus-activated killer (HAK) cells, have been continuously maintained for several months in tissue culture and these HAK cells contain multiple copies of stable circular viral episomes. The growth and cytotoxicity of HAK cells was found independent of IL-2. Analysis of deletion mutant infected cells suggests that at least two open reading frame sequences of a bicistronic mRNA encoded by the viral genome is involved in controlling IL-2 independence. This model could facilitate studies on growth regulation of human cytotoxic T cells that are important effector cells in immune responses against infectious diseases and cancer and should help us to elucidate the mechanism of transformation byH. saimirioncogenes.