Hollingsworth M A, Evans D L
J Natl Cancer Inst. 1984 Jun;72(6):1357-63.
New Zealand Black ( NBR ) rats that are innately immune to challenge with a syngeneic 3-methylcholanthrene [(MCA) CAS: 56-49-5]-induced fibrosarcoma have spleen cells that produce helper effects for in vitro lymphoproliferative responses in the presence of individual MCA-induced fibrosarcoma cells. Spleen cells from MCA-induced fibrosarcoma progressor rats (which lack innate tumor immunity) do not produce demonstrable helper activity. Supernatants from 48-hour cocultures of spleen cells from tumor-immune (TI) rats and syngeneic MCA-induced fibrosarcoma cells replaced the spleen cell helper activity. Comparable spleen cell supernatants from tumor progressor rats or unchallenged rats (controls) as well as supernatants from MCA-induced fibrosarcoma cells cultured alone did not produce any helper factor activity. Supernatants from TI rat spleen cells following inoculation with MCA-induced fibrosarcoma cells did not affect lymphoproliferative responses of NBR spleen cells induced by concanavalin A or alloantigens. The supernatants also did not contain detectable interleukin 2 activity as determined with the use of the thymocyte costimulator assay. These data indicate that the production of soluble helper factors by TI rat spleen cells may be involved in the augmentation of a protective host antitumor response.
对同基因3-甲基胆蒽[(MCA),化学物质登记号:56-49-5]诱导的纤维肉瘤攻击具有先天免疫的新西兰黑(NBR)大鼠,其脾细胞在单个MCA诱导的纤维肉瘤细胞存在的情况下,对体外淋巴细胞增殖反应产生辅助作用。来自MCA诱导的纤维肉瘤进展期大鼠(缺乏先天肿瘤免疫)的脾细胞不产生可证实的辅助活性。肿瘤免疫(TI)大鼠的脾细胞与同基因MCA诱导的纤维肉瘤细胞共培养48小时后的上清液替代了脾细胞的辅助活性。来自肿瘤进展期大鼠或未受攻击大鼠(对照)的类似脾细胞上清液,以及单独培养的MCA诱导的纤维肉瘤细胞的上清液均未产生任何辅助因子活性。用MCA诱导的纤维肉瘤细胞接种TI大鼠脾细胞后获得的上清液,不影响伴刀豆球蛋白A或同种异体抗原诱导的NBR脾细胞的淋巴细胞增殖反应。使用胸腺细胞共刺激试验测定,这些上清液也不含可检测到的白细胞介素2活性。这些数据表明,TI大鼠脾细胞产生可溶性辅助因子可能参与增强宿主的保护性抗肿瘤反应。