File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Selective functional deficit in dendritic cell - T cell interaction is a crucial mechanism in chronic hepatitis B virus infection
  • Basic View
  • Metadata View
  • XML View
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
 
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
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Zheng, BJ</contributor.author>
<contributor.author>Zhou, J</contributor.author>
<contributor.author>Qu, D</contributor.author>
<contributor.author>Siu, KL</contributor.author>
<contributor.author>Lam, TW</contributor.author>
<contributor.author>Lo, HY</contributor.author>
<contributor.author>Lee, SS</contributor.author>
<contributor.author>Wen, YM</contributor.author>
<date.accessioned>2010-09-06T07:50:17Z</date.accessioned>
<date.available>2010-09-06T07:50:17Z</date.available>
<date.issued>2004</date.issued>
<identifier.citation>Journal Of Viral Hepatitis, 2004, v. 11 n. 3, p. 217-224</identifier.citation>
<identifier.issn>1352-0504</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/79075</identifier.uri>
<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>
<language>eng</language>
<publisher>Blackwell Publishing Ltd.</publisher>
<relation.ispartof>Journal of Viral Hepatitis</relation.ispartof>
<rights>Journal of Viral Hepatitis. Copyright &#169; Blackwell Publishing Ltd.</rights>
<subject.mesh>Adult</subject.mesh>
<subject.mesh>Aged</subject.mesh>
<subject.mesh>Animals</subject.mesh>
<subject.mesh>Base Sequence</subject.mesh>
<subject.mesh>Case-Control Studies</subject.mesh>
<subject.mesh>Cell Communication</subject.mesh>
<subject.mesh>Cytokines - biosynthesis</subject.mesh>
<subject.mesh>DNA, Viral - genetics</subject.mesh>
<subject.mesh>Dendritic Cells - immunology</subject.mesh>
<subject.mesh>Female</subject.mesh>
<subject.mesh>Genes, MHC Class II</subject.mesh>
<subject.mesh>Hepatitis B Antibodies - blood</subject.mesh>
<subject.mesh>Hepatitis B Vaccines - administration &amp; dosage</subject.mesh>
<subject.mesh>Hepatitis B virus - genetics - isolation &amp; purification</subject.mesh>
<subject.mesh>Hepatitis B, Chronic - immunology - virology</subject.mesh>
<subject.mesh>Humans</subject.mesh>
<subject.mesh>Lymphocyte Activation</subject.mesh>
<subject.mesh>Male</subject.mesh>
<subject.mesh>Mice</subject.mesh>
<subject.mesh>Middle Aged</subject.mesh>
<subject.mesh>Monocytes - immunology</subject.mesh>
<subject.mesh>T-Lymphocytes - immunology</subject.mesh>
<title>Selective functional deficit in dendritic cell - T cell interaction is a crucial mechanism in chronic hepatitis B virus infection</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=1352-0504&amp;volume=11&amp;spage=217&amp;epage=224&amp;date=2004&amp;atitle=Selective+Functional+Deficit+in+Dendritic+CEll+-+T+Cell+interaction+Is+a+Crucial+Mechanism+in+Chronic+Hepatitis+B+Virus+Infection</identifier.openurl>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1111/j.1365-2893.2004.00497.x</identifier.doi>
<identifier.pmid>15117323</identifier.pmid>
<identifier.scopus>eid_2-s2.0-2442665419</identifier.scopus>
<identifier.hkuros>88002</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-2442665419&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>11</identifier.volume>
<identifier.issue>3</identifier.issue>
<identifier.spage>217</identifier.spage>
<identifier.epage>224</identifier.epage>
<identifier.isi>WOS:000221525300004</identifier.isi>
<publisher.place>United Kingdom</publisher.place>
</item>
Author Affiliations
  1. The University of Hong Kong
  2. Queen Elizabeth Hospital Hong Kong
  3. Fudan University Shanghai Medical College