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B亚群禽成髓细胞瘤相关病毒诱导鸡发生骨质硬化时,病毒DNA持续合成与巨噬细胞辅助细胞功能障碍的关联

Association of persistent synthesis of viral DNA with macrophage accessory cell dysfunction induced by avian retrovirus myeloblastosis-associated virus of subgroup B inducing osteopetrosis in chickens.

作者信息

Cummins T J, Smith R E

机构信息

Department of Microbiology, Colorado State University, Fort Collins 80523.

出版信息

Cancer Res. 1987 Nov 15;47(22):6033-9.

PMID:2444336
Abstract

This investigation concentrates on a regenerative anemia and immunosuppression occurring in the absence of osteopetrosis. Polyclonal activation of T-cells was used as an in vitro test system to study immunosuppression induced by the avian myeloblastosis-associated virus of Subgroup B inducing osteopetrosis [MAV-2(O)]. T-cell unresponsiveness in vitro was attributed to a defect in an accessory cell function of the macrophage. Counterflow centrifugation fractionation followed by mixing experiments indicated that the T-cell population from immunosuppressed chickens responded to mitogen stimulation when added to control macrophage cultures. In addition, lymphocyte fractions from uninfected chickens were unresponsive when added to macrophage cultures isolated from MAV-2(O)-infected chickens. Cultured splenic macrophages isolated from infected chickens contained high levels of both integrated and unintegrated viral DNA and formed syncytia by 21 days in culture. The macrophages remained viable and exhibited mature functional characteristics during mitogen stimulation assays. Therefore, it was speculated that the persistent synthesis of retrovirus DNA might be involved in the inability of infected macrophages to function as accessory cells.

摘要

本研究聚焦于在无骨质石化情况下发生的再生性贫血和免疫抑制。T细胞的多克隆激活被用作体外测试系统,以研究由诱导骨质石化的B亚群禽成髓细胞瘤相关病毒[MAV - 2(O)]诱导的免疫抑制。体外T细胞无反应性归因于巨噬细胞辅助细胞功能的缺陷。逆流离心分级分离随后进行混合实验表明,来自免疫抑制鸡的T细胞群体在添加到对照巨噬细胞培养物中时对有丝分裂原刺激有反应。此外,当将未感染鸡的淋巴细胞部分添加到从MAV - 2(O)感染鸡分离的巨噬细胞培养物中时,它们无反应。从感染鸡分离培养的脾巨噬细胞含有高水平的整合和未整合病毒DNA,并在培养21天时形成多核巨细胞。在有丝分裂原刺激试验期间,巨噬细胞保持存活并表现出成熟的功能特征。因此,推测逆转录病毒DNA的持续合成可能与感染的巨噬细胞无法作为辅助细胞发挥功能有关。

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