GENETICALLY CONTROLLED MECHANISMS OF RECOVERY FROM FRIEND VIRUS-INDUCED LEUKEMIA

成年小白鼠康复的遗传调控机制研究 Friend病毒复合体(FV)诱导的白血病显示H-2D亚区 似乎通过改变产生的动力学影响恢复 FV特异性辅助T淋巴细胞。此外，H-2内的基因(S) 发现复合体影响Fv诱导免疫抑制的能力 到非逆转录病毒抗原。这种对逆转录病毒的抵抗力 免疫抑制发生在存在病毒血症和持续性的情况下 白血病脾肿大。此外，免疫抑制不是被抑制的 Rfv-3r/S基因的存在使某些白血病小鼠 建立对FV的有效体液免疫应答。感染H-2a/a病毒的小鼠 Rfv-3r/S基因分型与艾滋病患者相似 产生了体液抗病毒抗体，但被免疫抑制以挑战 非病毒抗原。因此，对病毒和非病毒的免疫反应 在这个系统中，抗原似乎受到不同宿主基因的影响。 对控制这些免疫反应的因素的阐明应该是 对了解艾滋病患者的类似反应有价值。

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.