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Article: Selective functional deficit in dendritic cell - T cell interaction is a crucial mechanism in chronic hepatitis B virus infection

TitleSelective functional deficit in dendritic cell - T cell interaction is a crucial mechanism in chronic hepatitis B virus infection
Authors
Issue Date2004
PublisherBlackwell Publishing Ltd.
Citation
Journal Of Viral Hepatitis, 2004, v. 11 n. 3, p. 217-224 How to Cite?
AbstractA defect in specific T cell immunity has long been assumed to be the central mechanism of persistent Hepatitis B virus (HBV) infection. Recent studies on HBV transgenic mice have suggested, however, that functional deficit of dendritic cells (DC) was an underlying cause for the T cell dysfunction. The functions of monocyte-derived DC were determined by studying 75 subjects that included chronic hepatitis B patients with low or high HBV load; antibody to hepatitis B surface antigen (anti-HBs) positive individuals who had recovered completely from previous acute HBV infection; healthy donors who had received hepatitis B vaccination and were anti-HBs positive; and immunologically naïve to HBV or the vaccine individual. Impaired interactions between monocyte-derived DC and T cells were shown in chronic HBV infection patients, especially in those with active virus replication. The dysfunctions included: (i) failure of DC to increase human leukocyte antigen (HLA-II), B7 expression and interleukin-12 secretion in responses to hepatitis B surface antigen (HBsAg), (ii) defective induction of T cell proliferative response to HBsAg, (iii) failure to activate T cells to produce cytokines and (iv) deficit in the induction of antigen specific cytotoxic T lymphocytes (CTLs). In vitro treatment of DC with tumour necrosis factor-α improved HLA-II and B7 expression, as well as Th cell and CTL responses. It is concluded that defective DC-T cell interactions may account for the specific T cell immune defects in chronic HBV infection. Immunotherapy that aims at restoring DC functions could offer a new opportunity for effectively managing persistent HBV infections.
Persistent Identifierhttp://hdl.handle.net/10722/79075
ISSN
2014 Impact Factor: 3.909
2014 SCImago Journal Rankings: 1.506
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZheng, BJen_HK
dc.contributor.authorZhou, Jen_HK
dc.contributor.authorQu, Den_HK
dc.contributor.authorSiu, KLen_HK
dc.contributor.authorLam, TWen_HK
dc.contributor.authorLo, HYen_HK
dc.contributor.authorLee, SSen_HK
dc.contributor.authorWen, YMen_HK
dc.date.accessioned2010-09-06T07:50:17Z-
dc.date.available2010-09-06T07:50:17Z-
dc.date.issued2004en_HK
dc.identifier.citationJournal Of Viral Hepatitis, 2004, v. 11 n. 3, p. 217-224en_HK
dc.identifier.issn1352-0504en_HK
dc.identifier.urihttp://hdl.handle.net/10722/79075-
dc.description.abstractA defect in specific T cell immunity has long been assumed to be the central mechanism of persistent Hepatitis B virus (HBV) infection. Recent studies on HBV transgenic mice have suggested, however, that functional deficit of dendritic cells (DC) was an underlying cause for the T cell dysfunction. The functions of monocyte-derived DC were determined by studying 75 subjects that included chronic hepatitis B patients with low or high HBV load; antibody to hepatitis B surface antigen (anti-HBs) positive individuals who had recovered completely from previous acute HBV infection; healthy donors who had received hepatitis B vaccination and were anti-HBs positive; and immunologically naïve to HBV or the vaccine individual. Impaired interactions between monocyte-derived DC and T cells were shown in chronic HBV infection patients, especially in those with active virus replication. The dysfunctions included: (i) failure of DC to increase human leukocyte antigen (HLA-II), B7 expression and interleukin-12 secretion in responses to hepatitis B surface antigen (HBsAg), (ii) defective induction of T cell proliferative response to HBsAg, (iii) failure to activate T cells to produce cytokines and (iv) deficit in the induction of antigen specific cytotoxic T lymphocytes (CTLs). In vitro treatment of DC with tumour necrosis factor-α improved HLA-II and B7 expression, as well as Th cell and CTL responses. It is concluded that defective DC-T cell interactions may account for the specific T cell immune defects in chronic HBV infection. Immunotherapy that aims at restoring DC functions could offer a new opportunity for effectively managing persistent HBV infections.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Ltd.en_HK
dc.relation.ispartofJournal of Viral Hepatitisen_HK
dc.rightsJournal of Viral Hepatitis. Copyright © Blackwell Publishing Ltd.en_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshCell Communicationen_HK
dc.subject.meshCytokines - biosynthesisen_HK
dc.subject.meshDNA, Viral - geneticsen_HK
dc.subject.meshDendritic Cells - immunologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenes, MHC Class IIen_HK
dc.subject.meshHepatitis B Antibodies - blooden_HK
dc.subject.meshHepatitis B Vaccines - administration & dosageen_HK
dc.subject.meshHepatitis B virus - genetics - isolation & purificationen_HK
dc.subject.meshHepatitis B, Chronic - immunology - virologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLymphocyte Activationen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMonocytes - immunologyen_HK
dc.subject.meshT-Lymphocytes - immunologyen_HK
dc.titleSelective functional deficit in dendritic cell - T cell interaction is a crucial mechanism in chronic hepatitis B virus infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1352-0504&volume=11&spage=217&epage=224&date=2004&atitle=Selective+Functional+Deficit+in+Dendritic+CEll+-+T+Cell+interaction+Is+a+Crucial+Mechanism+in+Chronic+Hepatitis+B+Virus+Infectionen_HK
dc.identifier.emailZheng, BJ:bzheng@hkucc.hku.hken_HK
dc.identifier.emailZhou, J:jiezhou@hku.hken_HK
dc.identifier.authorityZheng, BJ=rp00353en_HK
dc.identifier.authorityZhou, J=rp01412en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1365-2893.2004.00497.xen_HK
dc.identifier.pmid15117323en_HK
dc.identifier.scopuseid_2-s2.0-2442665419en_HK
dc.identifier.hkuros88002en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2442665419&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue3en_HK
dc.identifier.spage217en_HK
dc.identifier.epage224en_HK
dc.identifier.isiWOS:000221525300004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridZheng, BJ=7201780588en_HK
dc.identifier.scopusauthoridZhou, J=7405550443en_HK
dc.identifier.scopusauthoridQu, D=7006530448en_HK
dc.identifier.scopusauthoridSiu, KL=7102312040en_HK
dc.identifier.scopusauthoridLam, TW=7202522868en_HK
dc.identifier.scopusauthoridLo, HY=7202085337en_HK
dc.identifier.scopusauthoridLee, SS=8612932400en_HK
dc.identifier.scopusauthoridWen, YM=7401776949en_HK

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