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猿猴免疫缺陷病毒(SIV)感染后早期,猕猴淋巴细胞中丝裂原驱动的增殖及细胞因子转录受损。

Impaired mitogen-driven proliferation and cytokine transcription of lymphocytes from macaques early after simian immunodeficiency virus (SIV) infection.

作者信息

Spring M, Bodemer W, Stahl-Hennig C, Nisslein T, Hunsmann G, Dittmer U

机构信息

Department of Virology and Immunology, German Primate Centre, Göttingen, Germany.

出版信息

Viral Immunol. 1997;10(2):65-72. doi: 10.1089/vim.1997.10.65.

Abstract

Altered cytokine transcription might play an important role in the pathogenesis of human immunodeficiency virus (HIV) infection in humans. The infection of rhesus macaques with simian immunodeficiency virus (SIV) provides a relevant animal model for HIV infection. Therefore, we evaluated the cyokine transcription of phytohemagglutinin (PHA)-stimulated lymphocytes in the early phase after infection of four rhesus macaques with pathogenic SIV-mac239. To determine transcription of interleukin (IL)-2, interferon (IFN)-gamma, IL-4, IL-6, and IL-10 we established a semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR). After inoculation with SIV, all monkeys became productively infected and developed an acquired immunodeficiency syndrome (AIDS) like disease. Infection was associated with a proliferation dysfunction of monkey lymphocytes in response to PHA. In addition, a decreasing overall cytokine transcription could be observed during the course of SIV infection. These findings demonstrate that an impairment of the lymphocyte function is associated with a reduced cytokine transcription in the early phase of an immunodeficiency virus infection. The observed differences of cytokine expression might contribute to the impaired immune response of SIV-infected monkeys and HIV-infected humans.

摘要

细胞因子转录改变可能在人类免疫缺陷病毒(HIV)感染人类的发病机制中起重要作用。恒河猴感染猿猴免疫缺陷病毒(SIV)为HIV感染提供了一个相关的动物模型。因此,我们评估了4只恒河猴感染致病性SIV-mac239后早期阶段,植物血凝素(PHA)刺激的淋巴细胞的细胞因子转录情况。为了确定白细胞介素(IL)-2、干扰素(IFN)-γ、IL-4、IL-6和IL-10的转录情况,我们建立了半定量逆转录聚合酶链反应(RT-PCR)。接种SIV后,所有猴子均发生有效感染,并发展为类似获得性免疫缺陷综合征(AIDS)的疾病。感染与猴子淋巴细胞对PHA反应的增殖功能障碍有关。此外,在SIV感染过程中可观察到总体细胞因子转录减少。这些发现表明,在免疫缺陷病毒感染的早期阶段,淋巴细胞功能受损与细胞因子转录减少有关。观察到的细胞因子表达差异可能导致SIV感染的猴子和HIV感染的人类免疫反应受损。

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