Ishihara C, Miyazawa M, Nishio J, Chesebro B
United States Department of Health and Human Services, National Institutes of Health, National Institute of Allergy and Infectious Diseases, Hamilton, MT 59840.
J Immunol. 1991 Jun 1;146(11):3958-63.
(B10.A x A/WySn)F1, H-2a/a, mice are genetic nonresponders to the envelope protein of Friend murine leukemia helper virus (F-MuLV) when immunized with a recombinant vaccinia virus expressing F-MuLV env gene. In contrast these mice can be protectively immunized against leukemogenic Friend virus complex using formalin-fixed F-MuLV virions in CFA. To determine which viral proteins were responsible for this immune protection, virion proteins prepared by SDS-PAGE and electroelution were used to immunize mice. Purified gp70 envelope protein in CFA was capable of inducing strong immune protection against the challenge with Friend virus complex in H-2a/a mice. Immunologic studies demonstrated that immunized mice developed a virus-specific T cell proliferative response and showed IgM to IgG Ig class switching of virus-neutralizing antibodies. These results indicated that genetically controlled immune nonresponsiveness to F-MuLV envelope Ag in H-2a/a mice could be overcome using denatured viral envelope protein together with a strong adjuvant.
（B10.A×A/WySn）F1、H-2a/a小鼠在用表达弗氏鼠白血病辅助病毒（F-MuLV）env基因的重组痘苗病毒免疫时，对F-MuLV包膜蛋白是基因无反应者。相比之下，使用CFA中经福尔马林固定的F-MuLV病毒粒子可对这些小鼠进行保护性免疫，使其抵抗致白血病性弗氏病毒复合物。为确定哪些病毒蛋白负责这种免疫保护，用SDS-PAGE和电洗脱制备的病毒粒子蛋白来免疫小鼠。CFA中的纯化gp70包膜蛋白能够诱导针对H-2a/a小鼠中弗氏病毒复合物攻击的强大免疫保护。免疫学研究表明，免疫小鼠产生了病毒特异性T细胞增殖反应，并显示出病毒中和抗体从IgM到IgG的Ig类转换。这些结果表明，使用变性病毒包膜蛋白和强佐剂可克服H-2a/a小鼠中对F-MuLV包膜抗原的基因控制的免疫无反应性。
