Macrophage activation for tumor cytotoxicity: induction of tumoricidal macrophages by supernatants of PPD-stimulated Bacillus Calmette-Guérin-immune spleen cell cultures.

Macrophage activation for tumor cytotoxicity: induction of tumoricidal macrophages by supernatants of PPD-stimulated Bacillus Calmette-Guérin-immune spleen cell cultures.
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肿瘤细胞毒性的巨噬细胞活化:通过 PPD 刺激的卡介苗免疫脾细胞培养物上清液诱导杀肿瘤巨噬细胞。

DOI:
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发表时间:
1977
影响因子:
4.4
通讯作者:
Monte S. Meltzer
Monte S. Meltzer
中科院分区:
医学2区
文献类型:
--
作者:
L. Ruco;Monte S. Meltzer

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通过与BCG 1免疫脾细胞和PPD共培养以及与PPD刺激的BCG免疫脾细胞培养物的上清液(淋巴因子上清液)孵育,激活正常小鼠的驻留腹腔巨噬细胞的体外肿瘤细胞毒性。巨噬细胞的吞噬因子激活发生在未分级的PC悬浮液以及在巨噬细胞单层耗尽的非粘附PC。由淋巴因子激活的巨噬细胞的肿瘤细胞毒性是明显的3至4小时的培养物中的活性上清液,达到最大水平的8至12小时。和不存在的20小时。在淋巴因子中继续孵育,甚至再曝光后洗涤没有保持巨噬细胞的细胞毒性。正常居民的巨噬细胞被激活的淋巴因子在体外的能力逐渐下降,并在培养20小时缺席。这种减少并不一定反映细胞死亡;通过排除台盼蓝或吞噬反应估计的巨噬细胞活力在20小时培养期间没有变化。巨噬细胞杀肿瘤能力和前体细胞被淋巴因子激活的能力的短暂性质可能在免疫反应中起负反馈机制的作用。
Resident peritoneal macrophages from normal mice were activated for tumor cytotoxicity in vitro by co-cultivation with BCG1-immune spleen cells and PPD and by incubation with supernatants of PPD-stimulated BCG-immune spleen cell cultures (lymphokine supernatants). Lymphokine activation of macrophages occurred in unfractionated PC suspensions as well as in macrophage monolayers depleted of nonadherent PC. Tumor cytotoxicity by lymphokine-activated macrophages was evident by 3 to 4 hr of culture in active supernatants, reached maximal levels by 8 to 12 hr. and was absent by 20 hr. Continued incubation in lymphokines or even re-exposure after washing did not maintain macrophage cytotoxicity. The capacity of normal resident macrophages to be activated by lymphokines in vitro progressively decreased and was absent by 20 hr in culture. This decrease did not necessarily reflect cell death; macrophage viability as estimated by exclusion of trypan blue or by phagocytic responses did not change over the 20-hr culture period. The short lived nature of both macrophage tumoricidal capacity and capacity of precursor cells to be activated by lymphokines may function as negative feedback mechanisms in immune reactions.