國家衛生研究院 NHRI:Item 3990099045/4714
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    题名: Lithium chloride modulate functions of human monocyte-derived dendritic cell
    作者: Leu, SJ;Liu, KJ;He, JZ;Lin, HC;Yang, YY;Shen, WW
    贡献者: National Institute of Cancer Research
    摘要: For almost half a century, lithium has been one of the most widelyused medications for bipolar depressive illness, although its therapeuticmechanism of action remains obscure. Accumulated preclinical andclinical evidences for the action of lithium in the brain suggest thatlithium can affect membrane transport systems, neurotransmitter receptorregulation, second messenger systems, protein kinase C (PKC) regulation,and gene expression. Recent studies showed long term, but not acute,treatment of cultured cerebellar granule cells with LiCl induce aconcentration-dependent decrease in proapoptotic p53 and Bax level;and remarkably increased cytoprotective Bcl-2 protein. These resultssuggest that lithium, in addition to its use in the treatment of bipolardepressive illness, may have an expanded use in improving neurodegeneration.However, regulation of lithium on the dendritic cell was not-welldefined. Dendritic cells (DC) are key regulators of immune responses, andwere involved in the initiation and maintenance of both innate and theadaptive immune responses. We demonstrate lithium chloride treatmentenhanced human monocyte-derived CD86 expression. In addition, lithiumchloride increased cytokines, TNF-a IL-8, IL-1b, IL-10 and IL-6production. However, lithium have no effect on T cell proliferationwhich assayed by mix lymphocyte reaction. These data suggest thatlithium chloride might modulate DC functions via phenotype andcytokines expression.
    日期: 2006-09
    關聯: Journal of Neuroimmunology. 2006 Sep;178(Suppl. 1):180.
    Link to: http://dx.doi.org/10.1016/j.jneuroim.2006.07.002
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0165-5728&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000241633101144
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