| HBcAg和HBeAg对小鼠骨髓源性树突状细胞功能的影响 |
| 投稿时间：2014-12-08 修订日期：2014-12-26 点此下载全文 |
| 引用本文：吴乐灿,蓝松松,吴金明,王秀燕,林贤凡,吴文治,黄智铭,吴建胜.HBcAg和HBeAg对小鼠骨髓源性树突状细胞功能的影响[J].医学研究杂志,2016,45(3):65-69 |
| DOI：
10.11969/j.issn.1673-548X.2016.03.018 |
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| 基金项目:浙江省自然科学基金资助项目(LY12H03003,Y2110768);温州市科技局科研基金资助项目(Y20140682) |
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| 中文摘要:目的 探讨HBcAg和HBeAg对小鼠骨髓源性树突状细胞功能的影响.方法 分离C57BL/6小鼠骨髓细胞,用rmGM-CSF和rmIL-4体外诱导为树突状细胞(DCs)后,按照干预条件分为对照组、HBcAg组和HBeAg组.混合淋巴细胞反应(MLR)检测DCs刺激T淋巴细胞增殖能力,酶联免疫法(ELISA)检测培养上清中IL-12、IL-10和IDO的分泌水平, Western blot法检测Akt 磷酸化水平,设置LY294002组为阳性对照探讨细胞因子分泌的可能调节机制.结果 HBcAg组上清液中IL-12水平以及DCs刺激淋巴细胞增殖能力较对照组明显升高(P<0.01).HBeAg组上清液中IL-12水平以及DCs刺激淋巴细胞增殖能力较对照组明显降低(P<0.05),而IL-10和IDO的水平较对照组明显升高(P<0.01).HBeAg组Akt的磷酸化水平较对照组明显升高(P<0.05).LY294002组Akt的磷酸化水平较HBeAg组明显降低(P<0.05),并且上清液中IL-12水平较HBeAg组明显升高(P<0.01),IL-10和IDO的水平较HBeAg组明显降低(P<0.01).结论 相对于HBcAg的正性作用,HBeAg通过PI3K-Akt信号通路调节DCs细胞因子分泌,减弱DCs的免疫功能,这可能是乙型肝炎慢性化的机制之一. |
| 中文关键词:乙型肝炎e抗原 乙型肝炎核心抗原 树突状细胞 吲哚胺2,3-双加氧化酶 Akt |
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| Effects of Hepatitis B Core Antigen and e Antigen on the Function of Mouse Bone Marrow-derived Dendritic Cells. |
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| Abstract:Objective To investigate the effects of hepatitis B core antigen and e antigen on the function of mouse bone marrow-derived dendritic cells. Methods Dendritic cells(DCs) were acquired from mouse bone marrow-derived cells by rmGM-CSF and rmIL-4. All the DCs were classified into the control group,HBcAg-stimulated group and HBeAg-stimulated group. Then T-cell stimulatory capacity of DCs was determined in an allogeneic mixed lymphocyte reaction (MLR). The productions of IL-12, IL-10 and IDO were assessed by ELISA. The western blot was performed to detect the phosphorylation of Akt. Additional LY294002 was used as a positive group to explore the potential mechanism of cytokines regulation. Results The expression of IL-12 and the stimulating T cell proliferation ability of DCs from HBcAg-stimulated group were significantly increased compared with the control group(P<0.01). The expression of IL-12 and the stimulating T cell proliferation ability of DCs from HBeAg-stimulated group were significantly decreased compared with the control group(P<0.05), whereas the secretions of IL-10 and IDO were significantly increased(P<0.01). The phosphorylation of Akt in HBeAg-stimulated group was significantly increased compared with the control group (P<0.05).When LY294002 being used to inhibit the phosphorylation of PI3K (upstream regulator of Akt), the phosphorylation of Akt and the secretions of IL-10 and IDO in HBeAg group were significantly decreased and the production of IL-12 was significantly increased. Conclusion In contrast to the positive effect of HBcAg, HBeAg may utilize PI3K-Akt signaling pathway to regulate cytokines secretion and suppress the immune response of DCs. |
| keywords:Hepatitis B e antigen Hepatitis B core antigen Dendritic cells Indoleamine-2,3-dioxygenase Akt |
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