免疫因子协同B7转导的肿瘤细胞对淋巴细胞的激活作用

ACTIVATION OF MURINE SPLEEN LYMPHOCYTES SYNERGISTICALLY INDUCED BY B7 CONSTIMULATORY MOLECULE AND IMMUNOLOGICAL FACTORS

目的研究Ｂ７分子与免疫因子之间的协同作用，探索非免疫原性肿瘤的免疫基因治疗。方法将Ｂ７┐１基因导入非免疫原性肿瘤细胞Ｂ１６，在ｍＲＮＡ和蛋白质水平证实Ｂ７的表达后，首先体外观察Ｂ７分子、抗ＣＤ３单克隆抗体（抗ＣＤ３ｍＡｂ）和白细胞介素２（ＩＬ┐２）对小鼠脾淋巴细胞激活的协同作用。结果活肿瘤细胞免疫的小鼠脾淋巴细胞的反应性优于灭活肿瘤细胞免疫的小鼠脾淋巴细胞的反应性。免疫３周的小鼠脾淋巴细胞的反应性优于免疫１周的小鼠脾淋巴细胞的反应性。在抗ＣＤ３ｍＡｂ和ＩＬ┐２单独或联合存在下，Ｂ７＋Ｂ１６比Ｂ７－Ｂ１６诱导明显增强小鼠脾淋巴细胞的增殖。

Objective:Activation of murine spleen lympyocytes synergistically induced by B7 molecules and immunological factors was studied to explore immuno gene therapy of nonimmunogenic tumor.Methods:Nonimmunogenic tumor cells B16 were transfected with murine B7 1 cDNA and expressed B7 at the level of mRNA and protein.First the synergistical role of B7 molecule,anti CD3 monoclonal antibody (mAb) and interleukin 2(IL 2) was observed in vitro for inducing the activation of murine spleen lymphocytes.Results:The responsibility of spleen lymphocytes from mice immunized by alive tumor cells was better than that from mice immunized by inactivated tumor cells.The responsibility of spleen lymphocytes from mice immunized for 3 weeks was better than that from mice immunized for 1 week.At the present of IL 2 and/or anti CD3 mAb,B7 +B16 as antigen presenting cells induced much stronger proliferation of murine spleen lymphocytes than B7 -B16 did.Conclusion:B7 costimulatory molecules expressed on nonimmunogenic tumor cells B16, anti CD3 mAb and IL 2 could synergistically induce the activation of murine spleen lymphocytes.This result could benefit further study.