H-2 compatibility requirement for virus-specific T cell-mediated effector functions in vivo. I. Specificity of T cells conferring antiviral protection against lymphocytic choriomeningitis virus is associated with H-2K and H-2D.
H-2 compatibility requirement for virus-specific T cell-mediated effector functions in vivo. I. Specificity of T cells conferring antiviral protection against lymphocytic choriomeningitis virus is associated with H-2K and H-2D.
复制标题
病毒特异性 T 细胞介导的体内效应功能的 H-2 兼容性要求。
DOI：
10.4049/jimmunol.117.5_part_1.1495
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发表时间：
1976
影响因子：
4.4
通讯作者：
R. Welsh
中科院分区：
文献类型：
--
作者：
R. Zinkernagel;R. Welsh
当在短期转移模型中进行检测时，预先感染淋巴细胞性脉络膜脑膜炎病毒(LCMV)的受体小鼠的过继免疫完全由病毒特异性胸腺来源的淋巴细胞介导。只有当免疫脾细胞的供者和受体共享H-2基因复合体的K或D区域时，才能获得保护，其衡量标准是减少脾中LCMV的空斑形成单位。I地区兼容性既不必要也不充分。F1导致的亲本组合与同基因系统一样有效。混合6倍的同种异体免疫细胞并不损害体内同种异体免疫脾细胞所发挥的保护作用。此外，体外加入同种异体系统的同种异体脾细胞或靶细胞不会抑制或抑制同种异体细胞的杀伤活性。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，这些小鼠定义了编码相关细胞表面结构的基因(S)。这些结果与以下观点是一致的，即针对病毒改变的细胞表面自身结构的免疫T细胞可能在感染病毒释放之前通过裂解靶细胞或通过淋巴因子施加的活动来损害体内的病毒生长。
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.