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[载脂蛋白A-I对树突状细胞表型和功能成熟的调节作用]

[Regulation on phenotypic and functional maturation of dendritic cells by apolipoprotein A-I].

作者信息

Xu Qi, Ma Hai-Mei, Ma Xiu-Min, Li Yu-Jiao, Zhao Hui, Kwak Jong-Young, Ding Jian-Bing

机构信息

Xinjiang Key Laboratory of The First Teaching Hospital of Xinjiang Medical University, Urumqi 830011, China.

出版信息

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2010 Oct;26(10):984-7.

Abstract

AIM

to investigate the effects of apolipoprotein A-I (ApoA-I) on the peripherial blood dendritic cell (PBDC) and monocyte derived DC (MDDC) in vitro.

METHODS

isolate PBDC or monocyte by cell isolation kit, monocyte were induced to MDDC by treated with GM-CSF plus IL-4 for 6 days, and then collect PBDC and MDDC treated them with apoA-I, LPS or TNF-α for 24 hours. Then check the cell surface marker and phagocytic capacity by flow cytometry. ELISA was used to detect the levels of cytokine secretion. T cells were stained with CFSE and T cell proliferation was assessed by flow cytometry.

RESULTS

collect the PBDC and MDDC with high purity. In the presence of ApoA-I, the surface markers on MDDC, such as CD40, CD86 and MHC-II, were up-regulated which were detected by flow cytometry. CD83 expression on both PBDC and MDDC was remarkably increased. ApoA-I DC demonstrated decreased the phagocytic capacity. ApoA-I also stimulated MDDC to produce IL-12 and TNF-α. Furthermore, ApoA-I can induce considerable Th cell proliferation.

CONCLUSION

ApoA-I can induce the maturation and activation of MDDC and PBDC, including the cytokine secretion, specific antigen presentation and T cell proliferation and decreasing the phagocytic capacity. Therefore, ApoA-I may attribute to the immune response in AS process.

摘要

目的

研究载脂蛋白A-I(ApoA-I)对体外外周血树突状细胞(PBDC)和单核细胞来源的树突状细胞(MDDC)的影响。

方法

用细胞分离试剂盒分离PBDC或单核细胞,单核细胞用GM-CSF加IL-4处理6天诱导为MDDC,然后收集PBDC和MDDC,用ApoA-I、LPS或TNF-α处理24小时。然后通过流式细胞术检测细胞表面标志物和吞噬能力。ELISA用于检测细胞因子分泌水平。T细胞用CFSE染色,通过流式细胞术评估T细胞增殖。

结果

收集到高纯度的PBDC和MDDC。在ApoA-I存在的情况下,流式细胞术检测发现MDDC表面标志物如CD40、CD86和MHC-II上调。PBDC和MDDC上的CD83表达均显著增加。ApoA-I处理的树突状细胞吞噬能力下降。ApoA-I还刺激MDDC产生IL-12和TNF-α。此外,ApoA-I可诱导显著的Th细胞增殖。

结论

ApoA-I可诱导MDDC和PBDC成熟和激活,包括细胞因子分泌、特异性抗原呈递和T细胞增殖,并降低吞噬能力。因此,ApoA-I可能参与动脉粥样硬化过程中的免疫反应。

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