GENETICALLY CONTROLLED MECHANISMS OF RECOVERY FROM FRIEND VIRUS-INDUCED LEUKEMIA

从朋友病毒引起的白血病中恢复的基因控制机制

• 批准号: 4688345
• 负责人: B W CHESEBRO
• 金额: --
• 依托单位: NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/4688345
• 关键词: Friend leukemia; Friend virus; T lymphocyte; antigen antibody reaction; antitumor antibody; antiviral antibody; cellular immunity; chronic disease /disorder; gene expression; helper T lymphocyte; histocompatibility antigens; histocompatibility gene; host neoplasm interaction; humoral immunity; immune response genes; immunofluorescence technique; immunogenetics; immunosuppression; major histocompatibility complex; microorganism immunology; molecular oncology; monoclonal antibody; neoplasm /cancer genetics; neoplasm /cancer immunology; neoplasm /cancer remission /regression; radioimmunoassay; tissue /cell culture; viral leukemia; virus antigen; virus diseases; virus genetics; virus related neoplasm /cancer

Studies of the mechanisms of genetic control of recovery of adult mice from Friend virus complex (FV)-induced leukemia revealed that the H-2D subregion appeared to influence recovery by altering the kinetics of generation of FV-specific helper T lymphocytes. In addition, gene(s) within the H-2 complex were found to affect the ability of FV to induce immunosuppression to non-retroviral antigens. This resistance to retrovirus-induced immunosuppression occurred in the presence of viremia and persistent leukemic splenomegaly. Furthermore, immunosuppression was not inhibited by the presence of the Rfv-3r/s genotype which enabled certain leukemic mice to mount an effective humoral immune response to FV. Mice with the H-2a/a and Rfv-3r/s genotypes appeared to be similar to AIDS patients in that they made humoral antiviral antibody but were immunosuppressed to challenge with nonviral antigens. Thus, the immune response to viral and nonviral antigens appeared to be influenced by separate host genes in this system. Elucidation of the factors controlling these immune responses should be of value in understanding similar responses in AIDS.

成年小鼠康复的遗传控制机制研究 Friend 病毒复合体 (FV) 诱导的白血病揭示了 H-2D 亚区 似乎通过改变生成动力学来影响恢复 FV 特异性辅助 T 淋巴细胞。 此外，H-2 内的基因 复合物被发现影响 FV 诱导免疫抑制的能力 针对非逆转录病毒抗原。 这种对逆转录病毒诱导的抵抗 免疫抑制发生在病毒血症存在且持续存在的情况下 白血病脾肿大。 此外，免疫抑制不被抑制 Rfv-3r/s 基因型的存在使得某些白血病小鼠能够 对 FV 产生有效的体液免疫反应。 带有 H-2a/a 的小鼠 Rfv-3r/s 基因型似乎与艾滋病患者相似，因为它们 产生了体液抗病毒抗体，但免疫抑制以挑战 非病毒抗原。 因此，对病毒和非病毒的免疫反应 抗原似乎受到该系统中单独宿主基因的影响。 应该阐明控制这些免疫反应的因素 对于了解艾滋病中的类似反应具有重要意义。