Modulation of the development of human monocyte-derived dendritic cells by lithium chloride.

Liu KJ; Lee YL; Yang YYShih NYHo CCWu YCHuang TSHuang MCLiu HCShen WWLeu SJ

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Modulation of the development of human monocyte-derived dendritic cells by lithium chloride.

机译：调制的人类的发展由锂monocyte-derived树突细胞氯。

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Lithium has been used or explored to treat psychiatric and neurodegenerative diseases that are frequently associated with an abnormal immune status. It is likely that lithium may work through modulation of immune responses in these patients. Because dendritic cells (DC) play a central role in regulating immune responses, this study investigated the influence of lithium chloride (LiCl) on the development and function of DC. Exposure to LiCl during the differentiation of human monocyte-derived immature DCs (iDC) enhances CD86 and CD83 expression and increases the production of IL-1beta, IL-6, IL-8, IL-10, and TNF-alpha. However, the presence of LiCl during LPS-induced maturation of iDC has the opposite effect. During iDC differentiation, LiCl suppresses the activity of glycogen synthase kinase (GSK)-3beta, and activates PI3K and MEK. In addition, LiCl activates peroxisome proliferator-activated receptor gamma (PPARgamma) during iDC differentiation, a pathway not described before. Each of these signaling pathways appears to have distinct impact on the differentiating iDC. The enhanced CD86 expression by LiCl involves the PI3K/AKT and GSK-3beta pathway. LiCl modulates the expression of CD83 in iDC mainly through MEK/ERK, PI3K/AKT, and PPARgamma pathways, while the increased production of IL-1beta and TNF-alpha mainly involves the MEK/ERK pathway. The effect of LiCl on IL-6/IL-8/IL-10 secretion in iDC is mediated through inhibition of GSK-3beta. We have also demonstrated that PPARgamma is downstream of GSK-3beta and is responsible for the LiCl-mediated modulation of CD86/83 and CD1 expression, but not IL-6/8/10 secretion. The combined influence of these molecular signaling pathways may account for certain clinical effect of lithium.

机译：锂或探索一直用于治疗精神病学和神经退行性疾病经常与异常免疫的地位。通过调制这些免疫反应病人。核心作用在调节免疫反应,这一点研究调查了锂的影响氯化(氯化锂)的开发和功能直流。分化的人类monocyte-derived不成熟的DCs (iDC)增强CD86和CD83表达和增加生产IL-1beta IL-6、IL-8 IL-10和TNF-alpha .然而,在LPS-induced氯化锂的存在iDC的成熟有相反的效果。iDC分化、氯化锂抑制活动糖原合酶激酶(GSK) 3β,和激活PI3K和MEK。激活过氧物酶体proliferator-activated在iDC受体γ(PPARgamma)分化,之前没有描述的一种途径。这些信号通路似乎区分iDC影响显著。氯化锂包括增强CD86表达PI3K / AKT GSK-3beta通路。在iDC CD83主要通过的表达PI3K / AKT, MEK / ERK和PPARgamma通路,而IL-1beta和增加产量tnf主要涉及MEK / ERK通路。氯化锂的影响il - 6 /引发/ il - 10分泌在iDC是通过抑制介导的GSK-3beta。PPARgamma GSK-3beta和下游负责LiCl-mediated调制CD86/83和CD1表达,但不是IL-6/8/10分泌。分子信号通路可能占锂的某些临床效果。

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来源
《Journal of Cellular Physiology》 |2011年第2期|424-433|共10页
作者
Liu KJ; Lee YL; Yang YYShih NYHo CCWu YCHuang TSHuang MCLiu HCShen WWLeu SJ;
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作者单位

National Institute of Cancer Research, National Health Research Institutes, Tainan, Taiwan.;

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正文语种英语
中图分类细胞生物学;
关键词
Glycogen Synthase Kinase 3 beta; Lithium; lithium chlorideCD83 geneDendritic CellsCD86 geneTumor Necrosis Factor-alphaPPAR gammaInterleukin-1beta;

机译：糖原合成酶激酶3β,锂,锂chlorideCD83 geneDendritic CellsCD86 geneTumor坏死Factor-alphaPPAR gammaInterleukin-1beta;

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Modulation of the development of human monocyte-derived dendritic cells by lithium chloride.

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