Leach D R, Callahan G N
Department of Pathology, Colorado State University, Fort Collins 80523, USA.
Pathobiology. 1995;63(2):57-64. doi: 10.1159/000163934.
A/JCr mice reject Sa1N fibrosarcoma cells genetically engineered to express major histocompatibility complex (MHC) class II molecules and are highly resistant to subsequent challenge with unmodified Sa1N cells. In this report we examine the mechanism by which this protective antitumor immunity is induced. We found that MHC class II antigen-positive tumor cells were no more effective than irradiated, MHC class II antigen-negative cells at inducing secondary protective immunity. Additionally, therapeutic immunization with MHC class II antigen-positive tumor cells had no effect on the growth of admixed Sa1N cells or preexisting Sa1N tumors. Based on these observations, we conclude that the MHC class II antigen-induced immune response is not related to Sa1N-specific antitumor immunity.
A/JCr小鼠能够排斥经过基因工程改造以表达主要组织相容性复合体（MHC）II类分子的Sa1N纤维肉瘤细胞，并且对随后用未修饰的Sa1N细胞进行的攻击具有高度抗性。在本报告中，我们研究了诱导这种保护性抗肿瘤免疫的机制。我们发现，MHC II类抗原阳性肿瘤细胞在诱导二次保护性免疫方面并不比经辐射的MHC II类抗原阴性细胞更有效。此外，用MHC II类抗原阳性肿瘤细胞进行治疗性免疫对混合的Sa1N细胞或预先存在的Sa1N肿瘤的生长没有影响。基于这些观察结果，我们得出结论，MHC II类抗原诱导的免疫反应与Sa1N特异性抗肿瘤免疫无关。
