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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, D3
Siu, KL1
Lam, TW2
Lo, HY2
Lee, SS1
Wen, YM3 3
 
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
2012 Impact Factor: 3.082
2012 SCImago Journal Rankings: 1.193
 
DOIhttp://dx.doi.org/10.1111/j.1365-2893.2004.00497.x
 
ISI Accession Number IDWOS:000221525300004
 
ReferencesReferences in Scopus
 
DC FieldValue
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
2012 Impact Factor: 3.082
2012 SCImago Journal Rankings: 1.193
 
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
 
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<description.abstract>A 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 na&#239;ve 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-&#945; 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.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong
  2. Queen Elizabeth Hospital Hong Kong
  3. Fudan University Shanghai Medical College