经OK-432活化的巨噬细胞对小鼠MM2肿瘤细胞系的抗体依赖细胞介导的细胞毒性。

Gan Pub Date : 1984-07-01
T Murayama
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引用次数: 0

摘要

探讨了OK-432诱导抗体依赖性巨噬细胞介导的细胞毒性(ADMC)对MM2癌细胞的作用机制。腹腔注射OK-432 4天后,从小鼠身上获得的粘附性腹膜渗出细胞(PEC)在抗血清存在的情况下,对MM2细胞表现出强大的细胞毒活性。抗血清来自无肿瘤小鼠,这些小鼠在接受OK-432治疗后存活超过60天,并抵抗MM2细胞的再攻击。抗thy -1.2和补体均未消除粘附的PEC的细胞毒活性,BALB/c小鼠粘附的PEC与无胸腺BALB/c (nu/nu)小鼠的ADMC无差异。此外,ADMC不仅对MM2细胞有活性,而且对其他异体肿瘤细胞(如MOPC-11浆细胞瘤细胞)也有活性。另一方面,通过蛋白a - sepharose CL-4B亲和柱消除抗MM2细胞血清中的有效因子。探讨了PEC和抗血清对MM2细胞的作用机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Antibody-dependent cell-mediated cytotoxicity against mouse MM2 tumor cell line by macrophages activated with OK-432.

The action mechanism of antibody-dependent macrophage-mediated cytotoxicity (ADMC) induced by OK-432 against MM2 carcinoma cells was examined. Adherent peritoneal exudate cells (adherent PEC) harvested from mice 4 days after intraperitoneal injection of OK-432 exhibited potent cytotoxic activity against MM2 cells in the presence of anti-serum obtained from tumor-free mice which had survived over 60 days following treatment with OK-432 and resisted rechallenge with MM2 cells. The cytotoxic activity of the adherent PEC was not abolished by treatment with anti-Thy-1.2 and complement, and there were no differences in ADMC between adherent PEC from BALB/c mice and those from athymic BALB/c (nu/nu) mice. Further, ADMC activity was shown not only against MM2 cells, but also against other allogeneic tumor cells, such as MOPC-11 plasmacytoma cells. On the other hand, the effective factor(s) in anti-serum to MM2 cells was eliminated by passage through a protein A-Sepharose CL-4B affinity column. The action mechanism of ADMC caused by the adherent PEC and anti-serum to MM2 cells is discussed.

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