Takeda Y, Tanaka M, Miyazaki H, Takeo S, Nomoto K, Yoshikai Y
Pharmaceutical Research Laboratories, Sapporo Breweries Ltd., Shizuoka, Japan.
Cancer Immunol Immunother. 1994 Mar;38(3):143-8. doi: 10.1007/BF01525634.
The growth of MethA tumor was significantly inhibited by oral administration of the alpha-glucan SPR-901 in BALB/c (+/+) mice but not in nude mice. Mice treated orally with SPR-901 exhibited an augmentation of antigen-specific resistance against rechallenge with the tumor cells. The tumor-neutralizing activity of regional lymph node cells from MethA-bearing mice against the tumor was augmented by oral administration of SPR-901. The tumor-neutralizing activity of lymph node cells from SPR-901-treated mice mainly appeared in Lyt2+ cells. Furthermore, lymphokine-activated killer activity of these cells was enhanced by administration of SPR-901. The antitumor effect of SPR-901 was abrogated in mice depleted of either L3T4+ or Lyt2+ cells, and in cyclosporin-A-treated mice. These results suggest that Lyt2+ cells are important effector cells in MethA-bearing mice orally administered SPR-901 and that functional exertion of both Lyt2+ and L3T4+ T cells is necessary for the antitumor effect of orally administered SPR-901 in vivo.
在BALB/c（+/+）小鼠中，口服α-葡聚糖SPR-901可显著抑制MethA肿瘤的生长，但在裸鼠中则无此效果。口服SPR-901的小鼠对肿瘤细胞再次攻击的抗原特异性抵抗力增强。口服SPR-901可增强荷MethA小鼠区域淋巴结细胞对肿瘤的中和活性。SPR-901处理小鼠的淋巴结细胞的肿瘤中和活性主要出现在Lyt2+细胞中。此外，给予SPR-901可增强这些细胞的淋巴因子激活的杀伤活性。在L3T4+或Lyt2+细胞耗竭的小鼠以及环孢素A处理的小鼠中，SPR-901的抗肿瘤作用被消除。这些结果表明，Lyt2+细胞是口服SPR-901的荷MethA小鼠中的重要效应细胞，并且Lyt2+和L3T4+ T细胞的功能发挥对于口服SPR-901在体内的抗肿瘤作用是必需的。
