Flt3配体对多器官功能障碍综合征小鼠脾脏树突状细胞及细胞免疫功能的修复作用

Flt3 ligand in recovering the function of the splenic dendritic cells and the immune system in mice with multiple organ dysfunction syndrome

目的探讨Flt3配体（FL）对多器官功能障碍综合征（MODS）晚期免疫失衡的修复作用与意义。方法按随机数字表法将90只实验鼠分为正常对照组、MODS组和FL治疗组，每组30只。用流式细胞技术检测各组脾脏树突状细胞（DC）、外周血单个核细胞主要组织相容性复合物Ⅱ类分子（I—A^b）表达变化及T细胞亚群变化，光、电镜下观察脾脏组织结构和DC变化。结果MODS组脾脏中未成熟DC明显增加（P〈0．05）；外周血单个核细胞I—A^b表达及CD4／CD8比值明显下降（P〈0．01和P〈0．05）；脾脏白髓消散，脾小体明显减少，DC多呈凋亡与退变崩解改变，周围淋巴细胞大量凋亡；活杀前动物死亡率为18％。治疗组小鼠脾脏中成熟DC数量明显增加（P〈0．05）；外周血单个核细胞I—A^b表达接近正常水平，CD4／CD8比值较MODS组明显上调；脾脏组织形态与DC的病理改变较MODS组明显减轻；实验鼠死亡率（7％）也明显降低。结论FL可以通过促进DC增生和活化，有效改善MODS晚期细胞免疫功能，进而缓解MODS的进程。

Objective To stduy the immunoprotective effect of fins-like tyrosine kinase receptor 3 ligand （FL） in multiple organ dysfunction syndrome （MODS） in mice. Methods Ninety mice were randomized into three groups： normal, MODS and MODS＋FL （each n=30）. The MODS model of mice was reproduced. Splenic dendritic cell （DC）, I-A^b of peripheral blood mononuclear cells （PBMCs） and T cell subpopulation of peripheral blood of mice were analyzed by flow cytometry. The histomorphology of spleen and DC was studied by light microscope and electron microscope. Results In MODS group, the number of splenic immature DC increased （P〈0.05）, the number of CD4^＋T lymphocytes reduced, while the number of CD8^＋T lymphoeytes increased, thus CD4/CD8 ratio was reduced （P〈0.05）. White pulp of the spleen dispersed, with decrease in splenic bodies. There was apoptosis of DC. The expression of I-A^b of the mononuclear cells decreased remarkably （P〈0.01）. The mortality of mice before treatment was 18%. In FL treatment groups, the number of splenic mature DC was markedly increased （P〈0.05）. The number of CD4^＋T lymphocytes and CD4/CD8 ratio was also markedly elevated. The expression of I-A^b of the mononuclear cells became normal. The pathological changes in spleen were alleviated. The mortality rate was significantly lowered （7%）. Conclusion FL can not only stimulate the recovery the DC activity, but also improve the immune function in the late phases of MODS.