论文部分内容阅读
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 vitamin D3 [1,25 (OH) 2 D3] and its analogs can inhibit the differentiation of human dendritic cells, but whether cell survival is regulated by the regulation of colony stimulating factor (CSF1) and its receptors. Methods Human peripheral blood mononuclear cells were differentiated into dendritic cells in vitro. The effects of 1,25 (OH) 2 D3 and its analogues on the expression of dendritic cells and the production of CSF 1 and its receptor were analyzed by flow cytometry, RT PCR and ELISA. Results 1,25 (OH) 2 D3 and tacalcitol significantly upregulated the expression of CSF 1 mRNA by dendritic cells and increased their protein secretion in a dose-dependent manner. However, the cell surface CSF 1 receptor and The expression of mRNA was inhibited. Solvent ethanol and 24, 25 (OH) 2 D3 had no effect on CSF 1 and its receptor. 1,25 (OH) 2 D3 had no effect on the expression of GM CSF receptor mRNA in dendritic cells. Conclusion The inhibition of dendritic cell differentiation by 1,25 (OH) 2 D3 is related to its specific regulation of CSF 1 and its receptor.