Uchiyama A, Morisaki T, Torisu M
Department of First Surgery, Kyushu University School of Medicine, Fukuoka, Japan.
Immunology. 1991 Sep;74(1):94-8.
The changes in the tumour-binding potential of human peripheral blood lymphocytes (PBL) after activation by interleukin-2 (IL-2) was investigated by directly counting the number of lymphocytes bound to lined hepatoma cell monolayers. A significant increase in the tumour-binding potential of PBL was found after activation by more than 100 U/ml of IL-2. Maximal tumour-binding potential was achieved at 1000 U/ml of activation, and an overdose of IL-2 activation slightly decreased this potential. These changes were almost exactly the same as the changes in anti-tumour cytotoxicity as measured by a 4-hr 51Cr-release assay. In addition, the kinetics of tumour binding by lymphokine-activated killer (LAK) cells was shown to be almost identical to that of tumour cell lysis. These results thus provide evidence that induction and regulation of LAK activity are mediated by changes in tumour-binding potential of lymphocytes after activation by IL-2.
通过直接计数与肝癌细胞单层结合的淋巴细胞数量，研究了白细胞介素-2（IL-2）激活后人外周血淋巴细胞（PBL）的肿瘤结合潜力变化。发现用超过100 U/ml的IL-2激活后，PBL的肿瘤结合潜力显著增加。在1000 U/ml的激活剂量下达到最大肿瘤结合潜力，而过量的IL-2激活会使这种潜力略有下降。这些变化与通过4小时51Cr释放试验测量的抗肿瘤细胞毒性变化几乎完全相同。此外，淋巴因子激活的杀伤细胞（LAK）与肿瘤结合的动力学显示与肿瘤细胞裂解的动力学几乎相同。因此，这些结果提供了证据，表明IL-2激活后淋巴细胞肿瘤结合潜力的变化介导了LAK活性的诱导和调节。
