Ashley M P, Kotlarski I, Hardy D
Immunology. 1977 Jan;32(1):1-10.
Immunization of mice with Salmonella enteritidis 11RX (11RX) induces resistance to tumour growth in these animals. The degree and duration of resistance is dependent on the routes used for immunization and tumour challenge. When resistance to tumour growth has declined, it can be recalled using various 11RX antigen preparations. In the present study we have shown that the ability to recall resistance to i.p. challenge with 131I-labelled Ehrlich ascites tumour cells could be transferred to normal mice by i.p. injection of an antigen preparation of 11RX mixed with spleen cells from 11RX-immunized mice. The active cells in this test were apparently sensitized T cells, since spleen cells from normal mice were not effective and the activity of immune spleen cells could be markedly reduced by removing theta antigen-bearing cells but not by removing glass-adherent cells. The induction of in vivo cytotoxicity appeared to depend on the involvement of radiation-sensitive cells derived from the non-immunized recipients, since recall of resistance to tumour challenge was reduced when irradiated mice were used as recipients of spleen cells from immunized mice.
用肠炎沙门氏菌11RX(11RX)免疫小鼠可诱导这些动物对肿瘤生长产生抗性。抗性的程度和持续时间取决于免疫和肿瘤攻击所采用的途径。当对肿瘤生长的抗性下降时,可使用各种11RX抗原制剂使其恢复。在本研究中,我们已表明,通过腹腔注射与来自11RX免疫小鼠的脾细胞混合的11RX抗原制剂,可将对腹腔注射131I标记的艾氏腹水瘤细胞攻击的抗性恢复能力转移至正常小鼠。该试验中的活性细胞显然是致敏T细胞,因为正常小鼠的脾细胞无效,并且通过去除携带θ抗原的细胞而非去除玻璃黏附细胞可显著降低免疫脾细胞的活性。体内细胞毒性的诱导似乎取决于来自未免疫受体的辐射敏感细胞的参与,因为当用受辐照小鼠作为免疫小鼠脾细胞的受体时,对肿瘤攻击的抗性恢复会降低。