File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Triptolide impairs dendritic cell migration by inhibiting CCR7 and COX-2 expression through PI3-K/Akt and NF-κB pathways

TitleTriptolide impairs dendritic cell migration by inhibiting CCR7 and COX-2 expression through PI3-K/Akt and NF-κB pathways
Authors
Issue Date2007
PublisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/molimm
Citation
Molecular Immunology, 2007, v. 44 n. 10, p. 2686-2696 How to Cite?
AbstractInhibition of dendritic cell (DC) migration into tissues and secondary lymphoid organs is an efficient way to induce immunosuppression and tolerance. CCR7 and PGE 2 are critical for DC migration to secondary lymphoid organs where DC initiate immune response. Triptolide, an active component purified from the medicinal plant Tripterygium Wilfordii Hook F., is a potent immunosuppressive drug capable of prolonging allograft survival in organ transplantation by inhibiting T cell activation and proliferation. Considering the essential role in T cell tolerance of DC migration to secondary lymphoid organs, here we demonstrate that triptolide can significantly inhibit LPS-triggered upregulation of CCR7 expression and PGE 2 production by inhibiting cyclooxygenase-2 (COX-2) expression in DC, thus impairing DC migration towards CCR7 ligand CCL19/MIP-3β in vitro. Moreover, triptolide-treated DC display impaired migration into secondary lymphoid organs and in vivo administration of triptolide also inhibits DC migration. Further studies show that the triptolide-mediated inhibitory effects of LPS-induced activation of phosphatidylinositol-3 kinase (PI3-K)/Akt and nuclear NF-κB activation are involved in down-regulation of COX-2 and CCR7 expression resulting in impaired migration to secondary lymphoid organs of DC. Therefore, inhibition of DC migration through decreasing COX-2 and CCR7 expression via PI3-K/Akt and NF-κB signal pathways provides additional mechanistic explanation for triptolide's immunosuppressive effect. © 2006 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/148500
ISSN
2015 Impact Factor: 3.375
2015 SCImago Journal Rankings: 1.524
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Qen_US
dc.contributor.authorChen, Ten_US
dc.contributor.authorChen, Gen_US
dc.contributor.authorShu, Xen_US
dc.contributor.authorSun, Aen_US
dc.contributor.authorMa, Pen_US
dc.contributor.authorLu, Len_US
dc.contributor.authorCao, Xen_US
dc.date.accessioned2012-05-29T06:13:20Z-
dc.date.available2012-05-29T06:13:20Z-
dc.date.issued2007en_US
dc.identifier.citationMolecular Immunology, 2007, v. 44 n. 10, p. 2686-2696en_US
dc.identifier.issn0161-5890en_US
dc.identifier.urihttp://hdl.handle.net/10722/148500-
dc.description.abstractInhibition of dendritic cell (DC) migration into tissues and secondary lymphoid organs is an efficient way to induce immunosuppression and tolerance. CCR7 and PGE 2 are critical for DC migration to secondary lymphoid organs where DC initiate immune response. Triptolide, an active component purified from the medicinal plant Tripterygium Wilfordii Hook F., is a potent immunosuppressive drug capable of prolonging allograft survival in organ transplantation by inhibiting T cell activation and proliferation. Considering the essential role in T cell tolerance of DC migration to secondary lymphoid organs, here we demonstrate that triptolide can significantly inhibit LPS-triggered upregulation of CCR7 expression and PGE 2 production by inhibiting cyclooxygenase-2 (COX-2) expression in DC, thus impairing DC migration towards CCR7 ligand CCL19/MIP-3β in vitro. Moreover, triptolide-treated DC display impaired migration into secondary lymphoid organs and in vivo administration of triptolide also inhibits DC migration. Further studies show that the triptolide-mediated inhibitory effects of LPS-induced activation of phosphatidylinositol-3 kinase (PI3-K)/Akt and nuclear NF-κB activation are involved in down-regulation of COX-2 and CCR7 expression resulting in impaired migration to secondary lymphoid organs of DC. Therefore, inhibition of DC migration through decreasing COX-2 and CCR7 expression via PI3-K/Akt and NF-κB signal pathways provides additional mechanistic explanation for triptolide's immunosuppressive effect. © 2006 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherPergamon. The Journal's web site is located at http://www.elsevier.com/locate/molimmen_US
dc.relation.ispartofMolecular Immunologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Movement - Drug Effectsen_US
dc.subject.meshChemokine CCl19en_US
dc.subject.meshChemokines, CC - Metabolismen_US
dc.subject.meshCyclooxygenase 2 - Metabolismen_US
dc.subject.meshCytokines - Metabolismen_US
dc.subject.meshDendritic Cells - Drug Effectsen_US
dc.subject.meshDinoprostone - Metabolismen_US
dc.subject.meshDiterpenes - Pharmacologyen_US
dc.subject.meshEpoxy Compounds - Pharmacologyen_US
dc.subject.meshImmunosuppressive Agents - Pharmacologyen_US
dc.subject.meshLipopolysaccharides - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshNf-Kappa B - Antagonists & Inhibitorsen_US
dc.subject.meshPhenanthrenes - Pharmacologyen_US
dc.subject.meshPhosphatidylinositol 3-Kinases - Antagonists & Inhibitorsen_US
dc.subject.meshProto-Oncogene Proteins C-Akt - Antagonists & Inhibitorsen_US
dc.subject.meshReceptors, CCr7en_US
dc.subject.meshReceptors, Chemokine - Antagonists & Inhibitors - Metabolismen_US
dc.titleTriptolide impairs dendritic cell migration by inhibiting CCR7 and COX-2 expression through PI3-K/Akt and NF-κB pathwaysen_US
dc.typeArticleen_US
dc.identifier.emailLu, L: liweilu@hkucc.hku.hken_US
dc.identifier.authorityLu, L=rp00477en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.molimm.2006.12.003en_US
dc.identifier.pmid17223196-
dc.identifier.scopuseid_2-s2.0-33846903837en_US
dc.identifier.hkuros126176-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33846903837&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume44en_US
dc.identifier.issue10en_US
dc.identifier.spage2686en_US
dc.identifier.epage2696en_US
dc.identifier.isiWOS:000245681200021-
dc.publisher.placeUnited Kingdomen_US
dc.customcontrol.immutablesml 130621-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats