Zinkernagel R M, Welsh R M
J Immunol. 1976 Nov;117(5 Pt 1):1495-502.
Adoptive immunization of recipient mice preinfected with lymphocytic choriomeningitis virus (LCMV) is mediated exclusively by virus-specific thymus-derived lymphocytes, when assayed in a short-term transfer model. Protection, measured as reduction of LCMV plaque-forming units in spleens, is conferred only if donors of immune spleen cells and recipients share the K or the D region of the H-2 gene complex. I region compatibility is neither necessary nor sufficient. The F1 leads to Parent combination is as effective as a syngeneic system. Admixture of a 6-fold excess of immune allogeneic cells did not impair the protective effect exerted by syngeneic immune spleen cells in vivo. Furthermore, allogeneic spleen cells or target cells added in syngeneic systems in vitro did not allogeneicly inhibit or suppress cytolytic activity. H-2 mutant mice B6. H-2bf did not protect wild type H-2Kb B10.A(5r) or vice versa. Therefore, these mice define the gene(s) coding for the relevant cell-surface structure involved. These results are consistent with the idea that immune T cells, which are specific for virally altered cell-surface self structures impair virus growth in vivo either by lysing target cells, probably before infectious virus is released, or alternatively via activities exerted by lymphokines.
在短期转移模型中进行检测时,对预先感染淋巴细胞性脉络丛脑膜炎病毒(LCMV)的受体小鼠进行过继免疫,完全由病毒特异性胸腺来源的淋巴细胞介导。以脾脏中LCMV空斑形成单位的减少来衡量的保护作用,只有在免疫脾细胞供体和受体共享H-2基因复合体的K或D区域时才会产生。I区域相容性既非必要条件也非充分条件。F1代与亲代的组合与同基因系统一样有效。加入6倍过量的免疫同种异体细胞并不损害同基因免疫脾细胞在体内发挥的保护作用。此外,在体外同基因系统中加入的同种异体脾细胞或靶细胞不会产生同种异体抑制或抑制细胞溶解活性。H-2突变小鼠B6.H-2bf不能保护野生型H-2Kb B10.A(5r),反之亦然。因此,这些小鼠确定了编码相关细胞表面结构的基因。这些结果与以下观点一致,即对病毒改变的细胞表面自身结构具有特异性的免疫T细胞,通过裂解靶细胞(可能在感染性病毒释放之前)或通过淋巴因子发挥的活性来损害体内病毒的生长。