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Article: BCG promotes cord blood monocyte-derived dendritic cell maturation with nuclear Rel-B up-regulation and cytosolic IκB α and β degradation

TitleBCG promotes cord blood monocyte-derived dendritic cell maturation with nuclear Rel-B up-regulation and cytosolic IκB α and β degradation
Authors
Issue Date2003
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/
Citation
Pediatric Research, 2003, v. 54 n. 1, p. 105-112 How to Cite?
AbstractMycobacterium bovis bacillus Calmette-Guerin (BCG) is given to millions of neonates in developing countries as a vaccine against Mycobacterium tuberculosis; however, little is known about the initiation of response in neonatal dendritic cells (DCs) to BCG. To address this issue, the interaction of BCG with human cord blood monocyte-derived DCs was studied. We showed that BCG could promote cord blood monocyte-derived DC maturation by up-regulation of CD80, CD83, CD86, CD40, and MHC class II molecules and down-regulation of mannose receptor. BCG was able to induce similar levels of tumor necrosis factor-α and IL-10 but no bioactive IL-12p70 production from cord blood DCs as from adult blood DCs. Functionally BCG-treated cord blood DCs had higher ability to induce mixed lymphocyte reaction than non-BCG-treated cord blood DCs. Both non-BCG-treated and BCG-treated cord blood DCs efficiently induced a high level of IL-10, medium level of interfer-on-γ, but little IL-4 production by cord blood naïve CD4+ T cells. Heat shock protein 65, a key component of BCG, had no effect on cord blood DC maturation in terms of CD86, MHC class II, and mannose receptor up-regulation. During the BCG-induced maturation process of cord blood DCs, nuclear transcription factor Rel-B was up-regulated and cytosolic Rel-B down-regulated with cytosolic IκB α and β degradation. These results suggest that BCG can promote cord blood monocyte-derived DC maturation, and that the mechanism is through the up-regulation of nuclear Rel-B secondary to the degradation of cytosolic IκB α and β.
Persistent Identifierhttp://hdl.handle.net/10722/170327
ISSN
2015 Impact Factor: 2.761
2015 SCImago Journal Rankings: 1.290
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Een_US
dc.contributor.authorLaw, HKWen_US
dc.contributor.authorLau, YLen_US
dc.date.accessioned2012-10-30T06:07:31Z-
dc.date.available2012-10-30T06:07:31Z-
dc.date.issued2003en_US
dc.identifier.citationPediatric Research, 2003, v. 54 n. 1, p. 105-112en_US
dc.identifier.issn0031-3998en_US
dc.identifier.urihttp://hdl.handle.net/10722/170327-
dc.description.abstractMycobacterium bovis bacillus Calmette-Guerin (BCG) is given to millions of neonates in developing countries as a vaccine against Mycobacterium tuberculosis; however, little is known about the initiation of response in neonatal dendritic cells (DCs) to BCG. To address this issue, the interaction of BCG with human cord blood monocyte-derived DCs was studied. We showed that BCG could promote cord blood monocyte-derived DC maturation by up-regulation of CD80, CD83, CD86, CD40, and MHC class II molecules and down-regulation of mannose receptor. BCG was able to induce similar levels of tumor necrosis factor-α and IL-10 but no bioactive IL-12p70 production from cord blood DCs as from adult blood DCs. Functionally BCG-treated cord blood DCs had higher ability to induce mixed lymphocyte reaction than non-BCG-treated cord blood DCs. Both non-BCG-treated and BCG-treated cord blood DCs efficiently induced a high level of IL-10, medium level of interfer-on-γ, but little IL-4 production by cord blood naïve CD4+ T cells. Heat shock protein 65, a key component of BCG, had no effect on cord blood DC maturation in terms of CD86, MHC class II, and mannose receptor up-regulation. During the BCG-induced maturation process of cord blood DCs, nuclear transcription factor Rel-B was up-regulated and cytosolic Rel-B down-regulated with cytosolic IκB α and β degradation. These results suggest that BCG can promote cord blood monocyte-derived DC maturation, and that the mechanism is through the up-regulation of nuclear Rel-B secondary to the degradation of cytosolic IκB α and β.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/en_US
dc.relation.ispartofPediatric Researchen_US
dc.rightsPediatric Research. Copyright © Lippincott Williams & Wilkins.-
dc.subject.meshAdulten_US
dc.subject.meshAntibodies - Pharmacologyen_US
dc.subject.meshBacterial Proteins - Pharmacologyen_US
dc.subject.meshCd4-Positive T-Lymphocytes - Metabolismen_US
dc.subject.meshCell Differentiationen_US
dc.subject.meshCell Divisionen_US
dc.subject.meshCell Nucleus - Metabolismen_US
dc.subject.meshChaperonin 60en_US
dc.subject.meshChaperonins - Pharmacologyen_US
dc.subject.meshCytosol - Metabolismen_US
dc.subject.meshDendritic Cells - Cytology - Metabolismen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshFetal Blooden_US
dc.subject.meshHistocompatibility Antigens Class Ii - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshI-Kappa B Proteins - Metabolismen_US
dc.subject.meshInterferon-Gamma - Metabolismen_US
dc.subject.meshInterleukin-10 - Blooden_US
dc.subject.meshInterleukin-12 - Blooden_US
dc.subject.meshInterleukin-4 - Metabolismen_US
dc.subject.meshMonocytes - Cytologyen_US
dc.subject.meshMycobacterium Bovisen_US
dc.subject.meshProtein Subunits - Blooden_US
dc.subject.meshProto-Oncogene Proteins - Metabolismen_US
dc.subject.meshTranscription Factor Relben_US
dc.subject.meshTranscription Factors - Metabolismen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Immunology - Metabolismen_US
dc.subject.meshUp-Regulationen_US
dc.titleBCG promotes cord blood monocyte-derived dendritic cell maturation with nuclear Rel-B up-regulation and cytosolic IκB α and β degradationen_US
dc.typeArticleen_US
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_US
dc.identifier.authorityLau, YL=rp00361en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1203/01.PDR.0000069703.58586.8Ben_US
dc.identifier.pmid12672905-
dc.identifier.scopuseid_2-s2.0-0038308879en_US
dc.identifier.hkuros80346-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0038308879&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume54en_US
dc.identifier.issue1en_US
dc.identifier.spage105en_US
dc.identifier.epage112en_US
dc.identifier.isiWOS:000183687000018-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLiu, E=7202240063en_US
dc.identifier.scopusauthoridLaw, HKW=7101939394en_US
dc.identifier.scopusauthoridLau, YL=7201403380en_US

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