从脐带血单核细胞来源树突状细胞(DC)表型变化的角度来探讨EB病毒对DC表型的影响,以阐明其逃逸宿主免疫的机制。将GM-CSF和IL-4、EB病毒和LPS不同组合对单核细胞来源DC进行刺激培养,利用单染色和三染色免疫荧光抗体标记一流式细胞术检测单核细胞来源DC表面CD14、CD11c、CD1a、HLA-DR、CD86、MR和MHCI类分子。加入EB病毒后,DC表面CD14分子表达的下调不明显,CD1a的表达则随病毒加入时细胞的分化阶段有关;同时EB病毒还影响了加入LPS后HLA-DR和CD86的升高和MR的降低;EB病毒还影响了细胞表面MHCI类分子的表达。因此EB病毒可抑制单核细胞来源DC的分化和成熟,这可能是其逃逸宿主免疫的机制之一。
To investigate the possible immune escape mechanism of EBV by exploring the phenotype changes during the differentiation and maturation of dendritic cells, the expression of CD11c, CD1a, HLA-DR, CD86, MR, MHC I molecules on the dendritic cells co-cultured with different combinations of GM-CSF, IL-4, EBV and LPS was tested by immunofluorescence staining and flow cytometry. After adding EBV, there were no significant changes on the expression of CD14 and CDllc on dendritic cells. However, the expression of CDla changed with the differentiation status of dendritic cells at that time. As for LPS induced DC maturation, EBV inhibited the increase of HLA-DR and CD86 and the decrease of MR. In addition, EBV significantly inhibited the expression of MHC I on dendritic cells. Thus it suggests that EBV can inhibit the differentiation and maturation of dendritic cells, which may be one of the mechanisms of EBV immunoescape.