B16 melanoma cells exposed in vitro to long-term IFN-alpha treatment (B16 alpha cells) as activators of tumor immunity in mice.
B16 melanoma cells exposed in vitro to long-term IFN-alpha treatment (B16 alpha cells) as activators of tumor immunity in mice.
复制标题
B16 黑色素瘤细胞在体外接受长期 IFN-α 治疗（B16 α 细胞）作为小鼠肿瘤免疫激活剂。
DOI：
10.1089/jir.1997.17.37
复制
发表时间：
1997
期刊：
影响因子：
--
通讯作者：
FleischmannJr,WR
中科院分区：
文献类型：
--
作者：
Fleischmann,CM;Wu,TY;FleischmannJr,WR
接种B16黑色素瘤细胞的小鼠暴露于长期体外干扰素-α处理（≥14天，B16α细胞），而不是短期体外干扰素-α处理（24小时），其存活时间延长。灭活的B16α细胞与活的B16α细胞同时接种可延长细胞的存活时间。此外，在活的B16细胞攻击之前接种灭活的B16α细胞，观察到生存时间的更大改善。小鼠接种灭活的、未经处理的B16细胞后，未观察到存活时间的延长。B16α细胞存活时间的延长与逆转录病毒表面抗原的表达无关。在B16α细胞、攻毒和IFN处理后存活的小鼠中，观察到对B16细胞的持久保护性免疫，而不是正常B16细胞。结果表明，接种灭活的B16α细胞，而不接种未处理的灭活B16细胞，能够显著延长小鼠同时或随后接受活B16细胞攻毒的存活时间。此外，接种b16 α而不接种b16的小鼠存活并伴有持久的免疫。接种灭活的b16α细胞可作为诱导宿主对亲代原发性或继发性肿瘤免疫的模型。
Mice inoculated with B16 melanoma cells exposed to long-termin vitroIFN-α treatment (≥14 days, B16α cells) but not short-termin vitroIFN-α treatment (24 h) exhibited an enhanced survival time. Enhanced survival time also occurred when inactivated B16α cells were inoculated at the same time as live B16 cells. Further, an even greater improvement in survival time was observed when the inactivated B16α cells were inoculated before live B16 cell challenge. No enhancement in survival time was observed when mice were inoculated with inactivated, untreated B16 cells. Enhancement of survival time by B16α cells was unrelated to retrovirus surface antigen expression. Long-lasting protective immunity to B16 cells was observed in mice that survived B16α cell, but not normal B16 cell, challenge and subsequent IFN treatment. It is evident that inoculation with inactivated B16α cells, but not with inactivated untreated B16 cells, was able to prolong significantly the survival time of mice either simultaneously or subsequently challenged with live B16 cells. Additionally, survival of B16α-inoculated but not B16-inoculated mice was accompanied by a durable immunity. Inoculation of inactivated B 16α cells may serve as a model for the induction of host immunity to a parental primary or secondary tumor.