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Article: Over-expression of Hlx homeobox gene in DC2.4 dendritic cell enhances its maturation and antigen presentation

TitleOver-expression of Hlx homeobox gene in DC2.4 dendritic cell enhances its maturation and antigen presentation
Authors
KeywordsAntigen presenting
Dendritic cell
Genetic modification
H2.0-like homebox
Issue Date2012
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ycimm
Citation
Cellular Immunology, 2012, v. 275 n. 1-2, p. 61-68 How to Cite?
AbstractHlx as a Th1-specific transcription factor, it appears to drive maturation of Th1 and IFN-γ secretion in cooperation with T-bet. In this study, we established a stable Hlx-over-expressed dendritic cell line (DC2.4/Hlx), and investigated the possible effect of Hlx gene on maturation of dendritic cell-line (DC2.4). Results shown that over-expressed Hlx in DC2.4 up-regulated the transcription and expression of IFN-γ, increased the expression of maturation makers including CD40, CD80, CD86, MHC-I and MHC-II. Functional assay for DC2.4/Hlx showed that over-expressed Hlx increased the expression level of interleukin-12 in the supernatant and decreased DC endocytosis when cells were incubated in vitro. Furthermore, using a syngeneic T cell activation model, we found that DC2.4/Hlx could obviously present ovalbumin (OVA) antigen to T cell in OVA pre-immunized mice.
Persistent Identifierhttp://hdl.handle.net/10722/164842
ISSN
2021 Impact Factor: 4.178
2020 SCImago Journal Rankings: 1.902
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorShotorbani, SS-
dc.contributor.authorHe, Z-
dc.contributor.authorYang, H-
dc.contributor.authorSun, Q-
dc.contributor.authorXu, Y-
dc.contributor.authorSu, Z-
dc.contributor.authorXue, Y-
dc.contributor.authorZheng, D-
dc.contributor.authorZhang, Y-
dc.contributor.authorWang, S-
dc.contributor.authorShao, Q-
dc.contributor.authorLu, L-
dc.contributor.authorXu, H-
dc.date.accessioned2012-09-20T08:10:47Z-
dc.date.available2012-09-20T08:10:47Z-
dc.date.issued2012-
dc.identifier.citationCellular Immunology, 2012, v. 275 n. 1-2, p. 61-68-
dc.identifier.issn0008-8749-
dc.identifier.urihttp://hdl.handle.net/10722/164842-
dc.description.abstractHlx as a Th1-specific transcription factor, it appears to drive maturation of Th1 and IFN-γ secretion in cooperation with T-bet. In this study, we established a stable Hlx-over-expressed dendritic cell line (DC2.4/Hlx), and investigated the possible effect of Hlx gene on maturation of dendritic cell-line (DC2.4). Results shown that over-expressed Hlx in DC2.4 up-regulated the transcription and expression of IFN-γ, increased the expression of maturation makers including CD40, CD80, CD86, MHC-I and MHC-II. Functional assay for DC2.4/Hlx showed that over-expressed Hlx increased the expression level of interleukin-12 in the supernatant and decreased DC endocytosis when cells were incubated in vitro. Furthermore, using a syngeneic T cell activation model, we found that DC2.4/Hlx could obviously present ovalbumin (OVA) antigen to T cell in OVA pre-immunized mice.-
dc.languageeng-
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ycimm-
dc.relation.ispartofCellular Immunology-
dc.subjectAntigen presenting-
dc.subjectDendritic cell-
dc.subjectGenetic modification-
dc.subjectH2.0-like homebox-
dc.titleOver-expression of Hlx homeobox gene in DC2.4 dendritic cell enhances its maturation and antigen presentation-
dc.typeArticle-
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1090-2163 (Electronic) 0008-8749 (Linkin&volume=275&issue=1-2&spage=61&epage=8&date=2012&atitle=Over-expression+of+Hlx+homeobox+gene+in+DC2.4+dendritic+cell+enhances+its+maturation+and+antigen+presentationen_US
dc.identifier.emailLu, L: liweilu@hkucc.hku.hk-
dc.identifier.authorityLu, L=rp00477-
dc.identifier.doi10.1016/j.cellimm.2012.02.016-
dc.identifier.pmid22483852-
dc.identifier.scopuseid_2-s2.0-84860595423-
dc.identifier.hkuros208157-
dc.identifier.volume275-
dc.identifier.issue1-2-
dc.identifier.spage61-
dc.identifier.epage68-
dc.identifier.isiWOS:000304509400010-
dc.publisher.placeUnited States-
dc.identifier.citeulike10469753-
dc.identifier.issnl0008-8749-

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