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细小病毒在哺乳动物细胞中诱导β干扰素、肿瘤坏死因子-α或白细胞介素-6的效率较低。

Parvoviruses are inefficient in inducing interferon-beta, tumor necrosis factor-alpha, or interleukin-6 in mammalian cells.

作者信息

Schlehofer J R, Rentrop M, Männel D N

机构信息

Angewandte Tumorvirologie, Heidelberg, Federal Republic of Germany.

出版信息

Med Microbiol Immunol. 1992;181(3):153-64. doi: 10.1007/BF00202055.

Abstract

To investigate a possible role of cytokines in parvovirus-mediated suppression of tumorigenesis, we tested in cell culture whether parvoviruses are able to induce interferon (IFN)-beta, tumor necrosis factor (TNF)-alpha or interleukin-6 (IL-6). Infection of rodent or human cells with the parvoviruses minute virus of mice (MVM), H-1 or adeno-associated virus (AAV) types 2 or 5 failed to induce expression of the luciferase or beta-galactosidase reporter genes transfected into these cells as constructs containing an IFN-beta promoter. Parvoviruses did weakly induce synthesis of TNF-alpha and of IL-6 in cell culture and could slightly enhance synthesis of these cytokines when induced by other agents. These in vitro data suggest that the rather unspecific tumor-suppressive properties of parvoviruses are unlikely to be attributable to stimulation of the synthesis of IFN, TNF or IL-6.

摘要

为了研究细胞因子在细小病毒介导的肿瘤发生抑制中的可能作用,我们在细胞培养中测试了细小病毒是否能够诱导干扰素(IFN)-β、肿瘤坏死因子(TNF)-α或白细胞介素-6(IL-6)。用细小病毒小鼠微小病毒(MVM)、H-1或2型或5型腺相关病毒(AAV)感染啮齿动物或人类细胞,未能诱导作为含有IFN-β启动子构建体转染到这些细胞中的荧光素酶或β-半乳糖苷酶报告基因的表达。细小病毒在细胞培养中确实能微弱地诱导TNF-α和IL-6的合成,并且当由其他试剂诱导时能稍微增强这些细胞因子的合成。这些体外数据表明,细小病毒相当非特异性的肿瘤抑制特性不太可能归因于对IFN、TNF或IL-6合成的刺激。

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