首页> 美国卫生研究院文献>Immunology >Evidence that induction and regulation of lymphokine-activated killer (LAK) activity are mediated by changes in tumour-binding potential of lymphocytes after activation by interleukin-2 (IL-2).
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Evidence that induction and regulation of lymphokine-activated killer (LAK) activity are mediated by changes in tumour-binding potential of lymphocytes after activation by interleukin-2 (IL-2).

机译:有证据表明白介素2(IL-2)激活后淋巴细胞的肿瘤结合潜能的变化介导了淋巴因子激活的杀手(LAK)活性的诱导和调节。

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摘要

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.
机译:通过直接计数与内衬的肝癌细胞单层结合的淋巴细胞的数量,研究了白介素2(IL-2)激活后人外周血淋巴细胞(PBL)的肿瘤结合潜力的变化。在激活超过100 U / ml的IL-2后,发现PBL的肿瘤结合潜力显着增加。激活1000 U / ml时可达到最大的肿瘤结合潜能,过量的IL-2激活会稍微降低这种潜能。这些变化与通过4小时51Cr释放测定法测得的抗肿瘤细胞毒性变化几乎完全相同。另外,淋巴因子激活的杀伤(LAK)细胞与肿瘤结合的动力学显示出与肿瘤细胞裂解几乎相同的动力学。因此,这些结果提供了证据,证明IL-2激活后淋巴细胞的肿瘤结合潜力的变化介导了LAK活性的诱导和调节。

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