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首页> 外文期刊>Clinical and Experimental Immunology: An Official Journal of the British Society for Immunology >'Danger' effect of low-density lipoprotein (LDL) and oxidized LDL on human immature dendritic cells.
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'Danger' effect of low-density lipoprotein (LDL) and oxidized LDL on human immature dendritic cells.

机译：低密度脂蛋白（LDL）和氧化LDL对人未成熟树突状细胞的“危险”效应。

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Dendritic cell (DC) maturation may accelerate autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis, and may contribute to accelerated atherosclerosis seen in these patients. The immune system responds to both exogenous and endogenous 'dangerous' signals that can induce dendritic cell maturation. We have found that autologous plasma contains danger signals that induce up-regulation of major histocompatibility complex (MHC) class II and co-stimulatory molecules in immature DCs (iDCs). The objective of this study was to determine whether low-density lipoprotein (LDL) and/or oxidized LDL (oxLDL) constitute danger signals, and to assess the effect of exposure to LDL and oxLDL following monocyte differentiation into iDCs in lipoprotein-deficient serum (LPDS). IDCs were generated in the presence of autologous plasma or LPDS. Expression of maturation and migration molecules was evaluated using flow cytometry, and morphology was assessed by light microscopy. Pro- or anti-apoptotic effect was determined using annexin V and propidium iodide binding. Phagocytosis of apoptotic cells was evaluated using autologous plasma or LPDS. LDL and oxLDL were clearly able to slightly up-regulate levels of HLA-DR and co-stimulatory molecule CD86. High oxLDL concentrations (50-100 microg/ml) were associated with expression of additional maturation molecules. Moreover, iDCs that were prepared in LPDS showed partial maturation following exposure to LDL and oxLDL, and improved tolerogenic apoptotic cell uptake. This study suggests that oxLDL, and to some extent LDL, are at least partly responsible for the iDC 'danger' response induced by autologous plasma.
机译：树突状细胞（DC）的成熟可能会加速自身免疫性疾病，例如系统性红斑狼疮和类风湿性关节炎，并可能导致这些患者的动脉粥样硬化加速。免疫系统对可诱导树突状细胞成熟的外源性和内源性“危险”信号均作出反应。我们已经发现自体血浆中含有危险信号，这些信号会诱导未成熟DC（iDC）中的主要组织相容性复合物（MHC）II类和共刺激分子上调。这项研究的目的是确定低密度脂蛋白（LDL）和/或氧化的LDL（oxLDL）是否构成危险信号，并评估在脂蛋白缺乏的血清中单核细胞分化为iDC后暴露于LDL和oxLDL的影响（ LPDS）。 IDC是在自体血浆或LPDS存在下产生的。使用流式细胞术评估成熟和迁移分子的表达，并通过光学显微镜评估形态。使用膜联蛋白V和碘化丙锭结合测定促凋亡作用或抗凋亡作用。使用自体血浆或LPDS评估凋亡细胞的吞噬作用。 LDL和oxLDL显然能够略微上调HLA-DR和共刺激分子CD86的水平。高oxLDL浓度（50-100微克/毫升）与其他成熟分子的表达有关。此外，在LPDS中制备的iDC在暴露于LDL和oxLDL后显示出部分成熟，并改善了耐受性凋亡细胞的摄取。这项研究表明，oxLDL和某种程度上的LDL至少部分负责自体血浆引起的iDC“危险”反应。

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