论文部分内容阅读
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。结论抗ＣＤ３ｍＡｂ和ＩＬ┐２可与非免疫原性肿瘤细胞表面表达的Ｂ７分子协同激活荷瘤小鼠的脾淋巴细胞
Objective To study the synergy between B7 molecule and immune factors and explore the immunogenic therapy of non-immunogenic tumors. Methods B7┐1 gene was introduced into non-immunogenic tumor cell B16. After B7 expression was confirmed at mRNA and protein levels, B7 molecule, anti-CD3 monoclonal antibody (anti-CD3 mAb) and interleukin 2 (IL┐2) were first observed in vitro. ) Synergistic effect on spleen lymphocyte activation in mice. Results The reactivity of splenic lymphocytes of mice immunized with live tumor cells was better than that of spleen lymphocytes of mice immunized with inactivated tumor cells. The reactivity of mouse splenic lymphocytes at 3 weeks of immunization was better than that of splenic lymphocytes from mice at 1 week of immunization. In the presence of anti-CD3 mAb and IL┐2 alone or in combination, B7+B16 induced significantly more proliferation of splenic lymphocytes in mice than B7-B16. Conclusion Anti-CD3 mAb and IL┐2 can synergistically activate the splenic lymphocytes of tumor-bearing mice with B7 molecules expressed on the surface of non-immunogenic tumor cells.