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

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TitleSelective functional deficit in dendritic cell - T cell interaction is a crucial mechanism in chronic hepatitis B virus infection
AuthorsZheng, BJ1
Zhou, J1
Qu, D
Siu, KL1
Lam, TW2
Lo, HY2
Lee, SS1
Wen, YM3
Issue Date2004
PublisherBlackwell Publishing Ltd.
CitationJournal Of Viral Hepatitis, 2004, v. 11 n. 3, p. 217-224 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1365-2893.2004.00497.x
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.
ISSN1352-0504
2011 Impact Factor: 4.088
2011 SCImago Journal Rankings: 0.375
DOIhttp://dx.doi.org/10.1111/j.1365-2893.2004.00497.x
ISI Accession Number IDWOS:000221525300004
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorZheng, BJ
dc.contributor.authorZhou, J
dc.contributor.authorQu, D
dc.contributor.authorSiu, KL
dc.contributor.authorLam, TW
dc.contributor.authorLo, HY
dc.contributor.authorLee, SS
dc.contributor.authorWen, YM
dc.date.accessioned2010-09-06T07:50:17Z
dc.date.available2010-09-06T07:50:17Z
dc.date.issued2004
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.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationJournal Of Viral Hepatitis, 2004, v. 11 n. 3, p. 217-224 [How to Cite?]
DOI: http://dx.doi.org/10.1111/j.1365-2893.2004.00497.x
dc.identifier.doihttp://dx.doi.org/10.1111/j.1365-2893.2004.00497.x
dc.identifier.epage224
dc.identifier.hkuros88002
dc.identifier.isiWOS:000221525300004
dc.identifier.issn1352-0504
2011 Impact Factor: 4.088
2011 SCImago Journal Rankings: 0.375
dc.identifier.issue3
dc.identifier.openurl
dc.identifier.pmid15117323
dc.identifier.scopuseid_2-s2.0-2442665419
dc.identifier.spage217
dc.identifier.urihttp://hdl.handle.net/10722/79075
dc.identifier.volume11
dc.languageeng
dc.publisherBlackwell Publishing Ltd.
dc.publisher.placeUnited Kingdom
dc.relation.ispartofJournal of Viral Hepatitis
dc.relation.referencesReferences in Scopus
dc.rightsJournal of Viral Hepatitis. Copyright © Blackwell Publishing Ltd.
dc.subject.meshAdult
dc.subject.meshAged
dc.subject.meshAnimals
dc.subject.meshBase Sequence
dc.subject.meshCase-Control Studies
dc.subject.meshCell Communication
dc.subject.meshCytokines - biosynthesis
dc.subject.meshDNA, Viral - genetics
dc.subject.meshDendritic Cells - immunology
dc.subject.meshFemale
dc.subject.meshGenes, MHC Class II
dc.subject.meshHepatitis B Antibodies - blood
dc.subject.meshHepatitis B Vaccines - administration & dosage
dc.subject.meshHepatitis B virus - genetics - isolation & purification
dc.subject.meshHepatitis B, Chronic - immunology - virology
dc.subject.meshHumans
dc.subject.meshLymphocyte Activation
dc.subject.meshMale
dc.subject.meshMice
dc.subject.meshMiddle Aged
dc.subject.meshMonocytes - immunology
dc.subject.meshT-Lymphocytes - immunology
dc.titleSelective functional deficit in dendritic cell - T cell interaction is a crucial mechanism in chronic hepatitis B virus infection
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Queen Elizabeth Hospital Hong Kong
  3. Fudan University Shanghai Medical College