Jorgensen P N
Scand J Immunol. 1975;4(4):373-82. doi: 10.1111/j.1365-3083.1975.tb02639.x.
Lymphoid cells of mice were sensitized in vivo either by H-2 strain-specific tumor allografts or by activation in lethally irradiated F1 hybrids and tested for cytotoxicity on 51Cr-labeled target cells. The release of 51Cr varied linearly with the logarithm to the proportion of effector lymphocytes to target cells and with the time of interaction. The release of 51Cr was immunologically specific and restricted to H-2 incompatibility. Spleen cells immune to public specificities of the target genotype were not cytotoxic. However, lymphoid cells immune to only one private specificity of a third-party target genotype were highly cytotoxic. The cytotoxicity of activated thymus cells on target cells sharing one private specificity with the genotype used for sensitization was significantly enhanced when the effector thymocytes were activated also against H-2 specificities not shared by the target strain. The results suggest that gene products that facilitate sensitization of effector cells may be determined both by the H-2K and the H-2D end of the H-2 complex. It remains to be shown whether the products of these loci, operating during sensitization in vivo, are body-wide correlated to the lymphocyte-defined specificities detectable during the mixed leukocyte culture interaction.
小鼠的淋巴细胞通过H-2品系特异性肿瘤同种异体移植在体内致敏，或通过在致死剂量照射的F1杂种中激活来致敏，并检测其对51Cr标记靶细胞的细胞毒性。51Cr的释放与效应淋巴细胞与靶细胞比例的对数以及相互作用时间呈线性关系。51Cr的释放具有免疫特异性，且仅限于H-2不相容性。对靶基因型公共特异性免疫的脾细胞没有细胞毒性。然而，仅对第三方靶基因型的一种私有特异性免疫的淋巴细胞具有高度细胞毒性。当效应胸腺细胞也针对靶菌株未共享的H-2特异性激活时，激活的胸腺细胞对与用于致敏的基因型共享一种私有特异性的靶细胞的细胞毒性显著增强。结果表明，促进效应细胞致敏的基因产物可能由H-2复合体的H-2K和H-2D端决定。这些位点的产物在体内致敏过程中起作用，是否与混合白细胞培养相互作用期间可检测到的淋巴细胞定义的特异性在全身相关，仍有待证明。
