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

Ko Jiunn Liu, Yueh Lun Lee, Yi Yuan Yang, Neng Yao Shih, Chia Chen Ho, Yu Chen Wu, Tze Sing Huang, Ming Chyi Huang, Hsing Cheng Liu, Winston W. Shen, Sy Jye Leu

研究成果: 雜誌貢獻文章

21 引文 (Scopus)

摘要

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-1β, IL-6, IL-8, IL-10, and TNF-α. 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)-3β, and activates PI3K and MEK. In addition, LiCl activates peroxisome proliferator-activated receptor γ (PPARγ) 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-3β pathway. LiCl modulates the expression of CD83 in iDC mainly through MEK/ERK, PI3K/AKT, and PPARγ pathways, while the increased production of IL-1β and TNF-α 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-3β. We have also demonstrated that PPARγ is downstream of GSK-3β 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.
原文英語
頁(從 - 到)424-433
頁數10
期刊Journal of Cellular Physiology
226
發行號2
DOIs
出版狀態已發佈 - 二月 2011

指紋

Lithium Chloride
Human Development
Dendritic Cells
Monocytes
Modulation
Glycogen Synthase Kinase 3
Peroxisome Proliferator-Activated Receptors
Mitogen-Activated Protein Kinase Kinases
Interleukin-8
Phosphatidylinositol 3-Kinases
Lithium
Interleukin-6
Interleukin-1
Interleukin-10
Neurodegenerative diseases
MAP Kinase Signaling System
Neurodegenerative Diseases
Psychiatry

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

引用此文

Modulation of the development of human monocyte-derived dendritic cells by lithium chloride. / Liu, Ko Jiunn; Lee, Yueh Lun; Yang, Yi Yuan; Shih, Neng Yao; Ho, Chia Chen; Wu, Yu Chen; Huang, Tze Sing; Huang, Ming Chyi; Liu, Hsing Cheng; Shen, Winston W.; Leu, Sy Jye.

於: Journal of Cellular Physiology, 卷 226, 編號 2, 02.2011, p. 424-433.

研究成果: 雜誌貢獻文章

Liu, Ko Jiunn ; Lee, Yueh Lun ; Yang, Yi Yuan ; Shih, Neng Yao ; Ho, Chia Chen ; Wu, Yu Chen ; Huang, Tze Sing ; Huang, Ming Chyi ; Liu, Hsing Cheng ; Shen, Winston W. ; Leu, Sy Jye. / Modulation of the development of human monocyte-derived dendritic cells by lithium chloride. 於: Journal of Cellular Physiology. 2011 ; 卷 226, 編號 2. 頁 424-433.
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abstract = "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-1β, IL-6, IL-8, IL-10, and TNF-α. 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)-3β, and activates PI3K and MEK. In addition, LiCl activates peroxisome proliferator-activated receptor γ (PPARγ) 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-3β pathway. LiCl modulates the expression of CD83 in iDC mainly through MEK/ERK, PI3K/AKT, and PPARγ pathways, while the increased production of IL-1β and TNF-α 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-3β. We have also demonstrated that PPARγ is downstream of GSK-3β 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.",
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AU - Lee, Yueh Lun

AU - Yang, Yi Yuan

AU - Shih, Neng Yao

AU - Ho, Chia Chen

AU - Wu, Yu Chen

AU - Huang, Tze Sing

AU - Huang, Ming Chyi

AU - Liu, Hsing Cheng

AU - Shen, Winston W.

AU - Leu, Sy Jye

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AB - 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-1β, IL-6, IL-8, IL-10, and TNF-α. 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)-3β, and activates PI3K and MEK. In addition, LiCl activates peroxisome proliferator-activated receptor γ (PPARγ) 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-3β pathway. LiCl modulates the expression of CD83 in iDC mainly through MEK/ERK, PI3K/AKT, and PPARγ pathways, while the increased production of IL-1β and TNF-α 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-3β. We have also demonstrated that PPARγ is downstream of GSK-3β 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.

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