Studies of the properties of a streptococcal preparation, OK-432 (NSC-B116209), as an immunopotentiator |
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Authors: | Tsugiya Murayama Shunnosuke Natsuume-Sakai Kazuo Ryoyama Saburo Koshimura |
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Affiliation: | (1) Department of Experimental Therapeutics, Cancer Research Institute, Kanazawa University, Takara-machi, 920 Kanazawa, Japan;(2) Department of Immunobiology, Cancer Research Institute, Kanazawa University, Takara-machi, 920 Kanazawa, Japan |
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Abstract: | Summary The present study was designed to examine the mechanism by which OK-432 triggers the cytotoxic activity of peritoneal exudate cells (PEC). When OK-432 was incubated with freshly harvested mouse serum, the formation of complexes of OK-432 with the third component of complement (C3) was demonstrated by using 131I-labeled mouse C3. The formation of C3-OK-432 complexes was totally abolished by a chelating compound, EDTA, which had been shown to inhibit the OK-432 induced activation of the alternative complement pathway. The C3-OK-432 complexes thus obtained bound to the resident PEC, which were subsequently shown to be activated. These activated PEC had augmented cytostatic activity against MM2 cells, a mouse mammary carcinoma.Further, the PEC from mice which had received an IP injection of OK-432 4–5 days previously were cytostatic against MM2 cells and also inhibited the growth of MM2 cells in culture. In contrast, resident PEC stimulated rather than inhibited the 3H-thymidine uptake by MM2 cells and the growth of MM2 cells. The mechanism of PEC (presumably macrophages) activation by OK-432 is discussed. |
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