GENETICALLY CONTROLLED MECHANISMS OF RECOVERY FROM FRIEND VIRUS-INDUCED LEUKEMIA

成年小鼠脑损伤恢复的遗传控制机制研究 Friend病毒复合体（FV）诱导的白血病显示，H-2D亚区 似乎影响回收率通过改变动力学的产生， FV特异性辅助T淋巴细胞。 此外，H-2中的基因 复合物影响FV诱导免疫抑制的能力 非逆转录病毒抗原。 这种对逆转录病毒诱导的 免疫抑制发生在存在病毒血症和持续 白血病性脾肿大 此外，免疫抑制不受 Rfv-3r/s基因型的存在使得某些白血病小鼠 对FV产生有效的体液免疫应答。 H-2a/a小鼠 Rfv-3r/s基因型与艾滋病患者相似， 产生抗病毒抗体，但免疫抑制攻击 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不同宿主基因的影响。 阐明控制这些免疫反应的因素应该是 对理解艾滋病中类似反应的价值。

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.