Shimoda K, Saito T, Kobayashi M, Nomoto K
First Department of Surgery, Medical College of Oita, Japan.
Biotherapy. 1992;5(1):63-9. doi: 10.1007/BF02194786.
Effects of a streptococcal preparation, OK-432, on precursors of lymphokine-activated killer (LAK) cells were observed in vivo. Total number of splenocytes and the ratio of asGM1+ cells increased gradually after i.v. administration of OK-432, reaching their peaks at 3 to 4 days. It was found that asGM1+ cells were nonadherent and large in size. There were little differences in the ratios of Thy-1+, Lyt-2+, and L3T4+ cells before and after OK-432 treatment. Mice were injected i.p. with recombinant interleukin 2 (rIL-2) at a dose of 5 x 10(4) U per mouse 4 days after OK-432 administration and LAK activity in their splenocytes was examined using natural killer (NK) resistant EL-4 target cells. Splenocytes in mice treated with both OK-432 and rIL-2 showed higher LAK activity than those in mice treated with rIL-2 alone. In vivo treatment with anti asGM1 antibody prior to rIL-2 injection abolished completely such augmentation of LAK activity in OK-432 treated mice. These results demonstrated that asGM1+ LAK precursor cells induced by OK-432 were effectively differentiated into LAK cells by rIL-2.
在体内观察了链球菌制剂OK-432对淋巴因子激活的杀伤细胞（LAK细胞）前体细胞的影响。静脉注射OK-432后，脾细胞总数和抗唾液酸化GM1（asGM1）阳性细胞比例逐渐增加，在3至4天时达到峰值。发现asGM1阳性细胞不黏附且体积较大。OK-432处理前后Thy-1阳性、Lyt-2阳性和L3T4阳性细胞的比例几乎没有差异。在给予OK-432 4天后，给小鼠腹腔注射剂量为每只小鼠5×10⁴单位的重组白细胞介素2（rIL-2），并使用对自然杀伤（NK）有抗性的EL-4靶细胞检测其脾细胞中的LAK活性。同时接受OK-432和rIL-2处理的小鼠的脾细胞显示出比单独接受rIL-2处理的小鼠更高的LAK活性。在注射rIL-2之前用抗asGM1抗体进行体内处理，完全消除了OK-432处理小鼠中LAK活性的这种增强。这些结果表明，OK-432诱导的asGM1阳性LAK前体细胞被rIL-2有效地分化为LAK细胞。
