摘要
目的 :研究巨噬细胞游走抑制因子 (MIF)基因修饰的 FBL 3红白血病细胞的生物学性质变化 ,为探讨其体内诱导抗肿瘤免疫反应的作用奠定基础。 方法 :以腺病毒介导 ,将 MIF基因导入小鼠 FBL 3红白血病细胞 ,观察其体外生物学性质变化。将 MIF基因修饰的 FBL 3细胞 (MIF- FBL 3)接种小鼠体内 ,观察其致瘤性和局部病理学变化 ,同时检测细胞因子 m RNA表达。 结果 :腺病毒能有效地将 MIF基因导入 FBL 3细胞 ,MIF的分泌可持续 10 d。 MIF- FBL 3细胞形态、增殖能力及表面MHC- ,MHC- ,B7- 1,B7- 2 ,ICAM- 1等分子的表达与野生型 FBL 3细胞相比无明显变化 ,但在小鼠体内的致瘤性降低 ,小鼠存活期延长 ,肿瘤局部可检测出 m TNF-α m RNA和 m L tn m RNA的表达 ,并有明显的单核和淋巴细胞浸润。 结论 :MIF-FBL 3细胞体外生物学性质无明显改变 ,但可能通过分泌 MIF在体内激活抗肿瘤免疫功能。
Objective: To study the role of MIF gene modified FBL3 erythroleukemia cells (MIF FBL3) in the induction of antitumor immune responses in vivo . The biologic characteristics of MIF FBL3 cell were investigated. Methods: The FBL3 cells were transfected by recombinant adenovirus with the gene encoding human MIF (AdexlhMIF). The biologic characteristics of MIF FBL3 were determined in vitro . The tumorigenicity of MIF FBL3 in vivo and the pathologic changes of tumor local tissues were observed after the mice were inoculated with MIF FBL3. The expression of cytokines mRNA in tumor local tissues was detected simultaneously. Results: The transfection efficiency of AdexlhMIF was high and MIF secretion of MIF FBL3 could last up to 10 days. Although no changes in the morphology, the proliferative ability and the expression of MHC Ⅰ, MHC Ⅱ, B7 1,B7 2, ICAM 1 molecules of MIF FBL3 were observed in vitro ,the tumorigenicity of MIF FBL3 decreased in vivo . The survival periods of the mice inoculated with MIF FBL3 were prolonged markedly. In the tumor local tissues of the mice inoculated with MIF FBL3, mTNF α mRNA and mLtn mRNA could be detected and the infiltration of monocytes and lymphocytes was obvious. Conclusion: The biologic characteristics of MIF FBL3 remain unchanged in vitro and the antitumor immune functions may be activated by MIF secreted from MIF FBL3 in vivo . [
出处
《第二军医大学学报》
CAS
CSCD
北大核心
2000年第8期727-730,F003,共5页
Academic Journal of Second Military Medical University
基金
国家自然科学基金!资助项目 (396 70 2 80 )
关键词
巨噬细胞游走抑制因子
基因修饰
红白血病细胞
microphage migration inhibitory factor
adenovirus
gene modification
erythroleukemia cell