English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 848030      Online Users : 713
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/4987


    Title: Modulation of the development of human monocyte-derived dendritic cells by lithium chloride
    Authors: Liu, KJ;Lee, YL;Yang, YY;Shih, NY;Ho, CC;Wu, YC;Huang, TS;Huang, MC;Liu, HC;Shen, WW;Leu, SJ
    Contributors: National Institute of Cancer Research
    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-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.
    Date: 2011-02
    Relation: Journal of Cellular Physiology. 2010 Feb;226(2):424-433.
    Link to: http://dx.doi.org/10.1002/jcp.22348
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0021-9541&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000286352600016
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=78649641162
    Appears in Collections:[黃智興] 期刊論文
    [劉柯俊] 期刊論文
    [施能耀] 期刊論文

    Files in This Item:

    File Description SizeFormat
    PUB20672290.pdf658KbAdobe PDF1677View/Open


    All items in NHRI are protected by copyright, with all rights reserved.

    Related Items in TAIR

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback