Please use this identifier to cite or link to this item: http://hdl.handle.net/11455/86425
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dc.contributor.authorWu, Chieh-Shanzh_TW
dc.contributor.authorLi, Yi-Rongzh_TW
dc.contributor.authorChen, Jeremy J Wzh_TW
dc.contributor.authorChen, Ying-Chezh_TW
dc.contributor.authorChu, Chiang-Liangzh_TW
dc.contributor.authorPan, I-Hongzh_TW
dc.contributor.authorWu, Yu-Shanzh_TW
dc.contributor.authorLin, Chi-Chenzh_TW
dc.date2014-
dc.date.accessioned2015-08-04T03:32:13Z-
dc.date.available2015-08-04T03:32:13Z-
dc.identifier.issn1090-2163zh_TW
dc.identifier.urihttp://hdl.handle.net/11455/86425-
dc.description.abstractDendritic cells (DCs) link the sensing of the environment by the innate immune system to the initiation of adaptive immune responses. Accordingly, DCs are considered to be a major target in the development of immunomodulating compounds. In this study, the effect of niclosamide, a Food and Drug Administration-approved antihelminthic drug, on the activation of lipopolysaccharide (LPS)-stimulated murine bone marrow-derived DCs was examined. Our experimental results show that niclosamide reduced the pro-inflammatory cytokine and chemokine expression of LPS-activated DCs. In addition, niclosamide also affected the expression of MHC and costimulatory molecules and influenced the ability of the cells to take up antigens. Therefore, in mixed cell cultures composed of syngeneic OVA-specific T cells and DCs, niclosamide-treated DCs showed a decreased ability to stimulate T cell proliferation and IFN-γ production. Furthermore, intravenous injection of niclosamide also attenuated contact hypersensitivity (CHS) in mice during sensitization with 2,4-dinitro-1-fluorobenzene. Blocking the LPS-induced activation of MAPK-ERK, JNK and NF-κB may contribute to the inhibitory effect of niclosamide on DC activation. Collectively, our findings suggest that niclosamide can manipulate the function of DCs. These results provide new insight into the immunopharmacological role of niclosamide and suggest that it may be useful for the treatment of chronic inflammatory disorders or DC-mediated autoimmune diseases.zh_TW
dc.language.isoenzh_TW
dc.relationCellular immunology, Volume 288, Issue 1-2, Page(s) 15-23.zh_TW
dc.subjectContact hypersensitivity (CHS)zh_TW
dc.subjectCytokinezh_TW
dc.subjectDendritic cellszh_TW
dc.subjectNiclosamidezh_TW
dc.subjectT cell proliferationzh_TW
dc.subjectAnimalszh_TW
dc.subjectAnthelminticszh_TW
dc.subjectBone Marrow Cellszh_TW
dc.subjectCell Proliferationzh_TW
dc.subjectCells, Culturedzh_TW
dc.subjectCoculture Techniqueszh_TW
dc.subjectDendritic Cellszh_TW
dc.subjectDinitrofluorobenzenezh_TW
dc.subjectFemalezh_TW
dc.subjectGene Expression Regulationzh_TW
dc.subjectHypersensitivityzh_TW
dc.subjectImmunizationzh_TW
dc.subjectImmunomodulationzh_TW
dc.subjectInjections, Intravenouszh_TW
dc.subjectLipopolysaccharideszh_TW
dc.subjectLymphocyte Activationzh_TW
dc.subjectMAP Kinase Kinase 4zh_TW
dc.subjectMicezh_TW
dc.subjectMice, Inbred C57BLzh_TW
dc.subjectMitogen-Activated Protein Kinase Kinaseszh_TW
dc.subjectNF-kappa Bzh_TW
dc.subjectNiclosamidezh_TW
dc.subjectSignal Transductionzh_TW
dc.subjectT-Lymphocyteszh_TW
dc.titleAntihelminthic niclosamide modulates dendritic cells activation and functionzh_TW
dc.typeJournal Articlezh_TW
dc.identifier.doi10.1016/j.cellimm.2013.12.006zh_TW
item.languageiso639-1en-
item.cerifentitytypePublications-
item.grantfulltextnone-
item.openairetypeJournal Article-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextno fulltext-
Appears in Collections:生物醫學研究所
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