小鼠急性CVB_(3m)心肌炎细胞免疫改变及rIL-2免疫干预的研究

The study of cell immunology and rIL 2 treatment in murine CVB3m myocarditis

目的探讨病毒性心肌炎小鼠细胞免疫的发病机理及早期给予重组白细胞介素２（ｒＩＬ２）在心肌炎中的作用。方法以柯萨奇病毒Ｂ３亲心肌变异株（ＣＶＢ３ｍ）诱导的ＢＡＬＢ／ｃ心肌炎小鼠为研究对象，观察小鼠脾脏Ｔ淋巴细胞亚群、自然杀伤细胞（ＮＫ）活性随病程的动态变化以及早期（０～５天）应用ｒＩＬ２治疗后上述指标的变化情况；并利用光镜观察了小鼠心脏及其它脏器的损伤情况。结果小鼠感染ＣＶＢ３ｍ后脾脏Ｔ淋巴细胞各亚群普遍下降，Ｌ３Ｔ＋４／Ｌｙｔ＋２上升，ＮＫ细胞活性一过性升高；而ｒＩＬ２治疗组Ｌ３Ｔ＋４、Ｌｙｔ＋２、Ｌ３Ｔ＋４／Ｌｙｔ＋２与正常对照组小鼠差异无显著意义，ＮＫ细胞活性于感染后２４小时迅速达高峰并持续在高水平。未治疗组小鼠病死率为３４％，ｒＩＬ２治疗组为１２％。结论细胞免疫在心肌炎发病中起重要作用。病毒性心肌炎早期应用ｒＩＬ２，可减轻心肌损害，降低感染动物的病死率，从而有效改善预后，为免疫治疗在心肌炎临床的应用提供了可能性。

Objective To explore the cell immunologic mechanism of viral myocarditis and determine the effects of rIL2 on CVB3 infected Balb/c mice Methods The spleen T lymphocyte subsets and NK cell activities in BALB/c mice with CVB3 myocarditis were observed, and compared with CVB3 myocarditis mice treated with rIL2 Results After the mice were infected with CVB3 the mice spleen T llymphocyte subsets decreased,L3T+4/Lyt+2 increased and NK cell activitis elevated temporarily However, the levels of L3T+4, Lyt+2 and L3T+4/Lyt+2 in myocarditis mice treated with rIL2 were not different from controls The NK cell activity in mice 24 hrs after infection reached the peak and steady level rapidly The mortalities of myocarditis mice with and without treatments were 12% and 34%, respectively Conclusion The cell immunology plays an important role in the pathogeneses of virusinduced myocarditis The application of rIL2 in the earle stage could decrease the lesions and mortality of CVB3 myocarditis