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目的研究HBeAg对小鼠骨髓源性树突状细胞(dendritic cell,DC)表型及功能的影响。方法以rmGM-CSF和rm IL-4定向体外诱导C57BL/6小鼠骨髓细胞分化成未成熟DC,随机分为空白对照组、HBeAg刺激组、脂多糖(LPS)刺激组和HBeAg+LPS刺激组。以流式细胞术检测DC表型变化,混合淋巴反应(MLR)检测DC促T淋巴细胞增殖能力,酶联免疫法(ELISA)检测细胞上清液中IL-12的分泌水平,CCK-8法检测HBeAg对骨髓源性树突状细胞活力影响。结果 HBeAg刺激后,CD11c阳性细胞百分数下降。HBeAg可抑制DC表面MHC-Ⅱ、CD86的表达和DC促淋巴细胞增殖的能力,且HBeAg可抑制LPS诱导的树突状细胞IL-12的分泌,细胞活力检测显示HBeAg对细胞没有明显毒性作用。结论 HBeAg对树突状细胞的成熟有一定的负性调节作用,这可能是HBV的持续感染的机制之一。
Objective To study the effect of HBeAg on the phenotype and function of mouse bone marrow-derived dendritic cells (DCs). Methods Bone marrow cells of C57BL / 6 mice were induced to differentiate into immature DCs induced by rmGM-CSF and rm IL-4 in vitro. They were randomly divided into blank control group, HBeAg stimulation group, LPS stimulation group and HBeAg + LPS stimulation group . The changes of DC phenotypes were detected by flow cytometry. The proliferation of DCs promoting T lymphocytes was detected by mixed lymphocyte reaction (MLR). The levels of IL-12 in supernatants were detected by enzyme-linked immunosorbent assay (ELISA) The effect of HBeAg on the activity of bone marrow-derived dendritic cells was detected. Results After HBeAg stimulation, the percentage of CD11c positive cells decreased. HBeAg can inhibit the expression of MHC-Ⅱ and CD86 on DCs and the ability of DCs to promote lymphocyte proliferation. HBeAg can inhibit the secretion of IL-12 by LPS-induced dendritic cells. HBeAg showed no obvious cytotoxic effect on cells. Conclusion HBeAg negatively regulates the maturation of dendritic cells, which may be one of the mechanisms of persistent HBV infection.