GENETICALLY CONTROLLED MECHANISMS OF RECOVERY FROM FRIEND VIRUS-INDUCED LEUKEMIA

这项工作的主要目的是研究基因控制 参与保护性免疫的宿主防御机制和 从Friend逆转录病毒复合体(FV)诱导的恢复 小鼠红白血病作为人类逆转录病毒病模型的研究 比如艾滋病和白血病。 我们延续了以前对H-2影响的研究 FV诱导的免疫抑制和保护作用的基因分型 对FV的免疫力。初步结果表明，患有AFP的小鼠 对逆转录病毒诱导的免疫抑制的高度敏感性可能 不受重组牛痘疫苗免疫的保护 表达FV囊膜基因产物。然而，H-2的使用 重组小鼠表明保护性免疫是 受H-2K和I-A亚区的影响，而 免疫抑制受H-2D亚区的影响。因此， 即使在高致病性的小鼠中也能诱导保护性免疫。 对FV诱导的免疫抑制的敏感性。这些结果 这表明在基因上更容易受到 HIV感染的免疫抑制作用可能仍然是 用适当的疫苗预防艾滋病。 最近对这种保护机制的研究更多。 系统表明，接种疫苗会诱导FV特异性T细胞 淋巴细胞启动。通过Fv挑战进行后续曝光 诱导细胞毒性T淋巴细胞和继发性体液 抗病毒抗体反应，这两种反应都可能参与 从疾病中恢复。

The main aim of this work is the study of genetically controlled host defense mechanisms involved in protective immunity and recovery from Friend retrovirus complex (FV)-induced erythroleukemia in mice as a model for human retrovirus diseases such as AIDS and leukemia. We have continued previous studies of the influences of H-2 genotype on both FV-induced immunosuppression and protective immunity against FV. Initial results suggested that mice with a high susceptibility to retrovirus induced immunosuppression could not be protected by immunization with a vaccinia recombinant expressing the FV envelope gene product. However, use of H-2 recombinant mice indicated that protective immunity was influenced by the H-2K and I-A subregions, whereas immunosuppression was influenced by the H-2D subregion. Thus, protective immunity was induced even in mice with high susceptibility to FV-induced immunosuppression. These results suggest that humans who are genetically more susceptible to the immunosuppressive effects of HIV infection might still be protected from AIDS with appropriate vaccines. More recent studies on the mechanism of protection in this system indicate that vaccination induces FV-specific T lymphocyte priming. Subsequent exposure by challenge with FV induces cytotoxic T lymphocytes and a secondary humoral antiviral antibody response, both of which may be involved in recovery from disease.