Brunner K T, Mauel J, Cerottini J C, Chapuis B
Immunology. 1968 Feb;14(2):181-96.
The cytotoxic effect of spleen cells of mice immunized by tumour allografts was studied by measuring target cell inactivation as a function of release of radioactive label (Cr) or loss of cloning efficiency. When sensitized lymphoid cells were incubated with target cells at a ratio of 100:1, up to 90 per cent of the incorporated label was released within 6–9 hours, while the number of clone-forming cells was reduced by up to 99 per cent in the same time period. Isoantiserum from the graft recipients, as well as its 19S and 7S fractions, protected target cells against the toxic effect of the spleen cells, but a lipoprotein antigen isolated from the tumour cells failed to inhibit the cytotoxic reaction. Target cell lysis as measured by specific release of Cr was partially inhibited by actinomycin-D and by cycloheximide at concentrations which effectively blocked DNA-dependent RNA and protein synthesis.
通过测量作为放射性标记（铬）释放或克隆效率损失函数的靶细胞失活，研究了经肿瘤同种异体移植免疫的小鼠脾细胞的细胞毒性作用。当致敏淋巴细胞与靶细胞以100:1的比例孵育时，在6 - 9小时内，高达90%掺入的标记被释放，而在同一时间段内，克隆形成细胞的数量减少高达99%。来自移植受体的同种抗血清及其19S和7S组分可保护靶细胞免受脾细胞的毒性作用，但从肿瘤细胞中分离出的脂蛋白抗原未能抑制细胞毒性反应。通过铬的特异性释放测量的靶细胞裂解，在有效阻断DNA依赖性RNA和蛋白质合成的浓度下，被放线菌素-D和环己酰亚胺部分抑制。
