摘要
目的 探讨维生素D3[1,2 5 (OH) 2 D3]及其类似物抑制人树突状细胞分化 ,但保持细胞生存是否通过调节集落刺激因子 (CSF 1)及其受体来实现。方法 在体外将人外周血单核细胞分化成树突状细胞。采用流式细胞术、RT PCR和ELISA法分析 1,2 5 (OH) 2 D3及其类似物对树突状细胞表达和产生CSF 1及其受体的作用。结果 1,2 5 (OH) 2 D3和他骨化醇 (tacalcitol)以剂量依赖的方式显著上调树突状细胞对CSF 1mRNA的表达 ,并增高其蛋白分泌水平 ,而细胞表面CSF 1受体以及mRNA的表达均受到抑制。溶剂乙醇和 2 4 ,2 5 (OH) 2 D3对CSF 1及其受体均无调节作用。 1,2 5 (OH) 2 D3对树突状细胞表达GM CSF受体mRNA无影响。结论 1,2 5 (OH) 2 D3对树突状细胞分化的抑制与其特异性地调节CSF 1及其受体有关。
Objective To investigate whether the inhibitory activity of vitamin D_3[1,25(OH)_2D_3] on dendritic cells differentiation without altering survival is mediated via its modulation of CSF-1 and its receptor. Methods Dendritic cells were harvested by differentiating human monocytes in vitro . Flow cytometry, RT-PCR and ELISA were used to analyze the effect of 1,25(OH)_2D_3 and its analogues on the expression and production of CSF-1 and its receptor. Results 1,25(OH)_2D_3 and tacalcitol significantly up-regulated CSF-1 mRNA expression and protein secretion in a dose-dependent manner. In contrast, CSF-1R mRNA- and cell surface-expression were simultaneously down-regulated. The solvent ethanol and 24,25(OH)_2D_3 didn′t show any effect. GM-CSF receptor mRNA expression was not modulated in 1,25(OH)_2D_3-treated cells. Conclusion Inhibition of dendritic cell differentiation without altering cell survival with 1,25(OH)_2D_3 may be explained by its specific modulatory role of CSF-1 and its receptor.
出处
《中华微生物学和免疫学杂志》
CAS
CSCD
北大核心
2003年第9期712-716,共5页
Chinese Journal of Microbiology and Immunology
基金
国家教委留学回国人员基金资助项目
浙江省医药卫生科学研究基金资助项目 (编号 :2 0 0 0A119)
