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Article: Lymphocyte subsets in renal allograft recipients with chronic hepatitis C virus infection

TitleLymphocyte subsets in renal allograft recipients with chronic hepatitis C virus infection
Authors
KeywordsHepatitis C
Lymphocyte
Natural killer cell
Renal transplantation
Issue Date1999
PublisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/
Citation
Nephrology Dialysis Transplantation, 1999, v. 14 n. 3, p. 717-722 How to Cite?
AbstractBackground. The pathogenetic mechanisms of chronic hepatitis C virus (HCV) infection in renal allograft recipients are not well established. This study aimed to examine the relationship between altered immune status and HCV-related liver disease, by determining the changes in peripheral blood lymphocyte and natural killer (NK) cell subsets in these subjects. Methods. Peripheral blood lymphocyte, NK cell and activation markers were detected by flow cytometry in renal allograft recipients with (TpC+) or without (TpC-) HCV infection, and compared with age- and sex-matched patients with post-transfusional chronic HCV infection (TfC+) and healthy controls. Results. CD19+ cells were reduced in renal allograft recipients compared with controls. TpC+ subjects had increased CD3+CD8+ cells compared with controls, and increased CD3+DR+ cells but reduced CD4+CD38+ and CD3-CD16/56+ cells compared with controls as well as TfC+ patients. TfC+ patients and controls had similar numbers and proportions for the lymphocyte subsets and NK cells. Chronic liver disease in HCV-infected renal allograft recipients was associated with increased CD3+CD16/56+ cells but reduced CD4+CD38+ cells. Reduction of CD3-CD16/56+ cells was noted in TpC+ subjects without liver disease. Yet among post-transfusional (TfC+) subjects this was associated with chronic hepatitis. Conclusions. Peripheral blood suppressor/cytotoxic T lymphocytes are increased, whereas activated helper/inducer T lymphocytes and NK cells are reduced, in renal allograft recipients with HCV infection. Increased non-MHC-restricted cytotoxic T cells and reduced NK cells are associated with the presence or absence of liver disease respectively. These data suggest that immune mechanisms are important in the pathogenesis of chronic hepatitis C after renal transplantation.
Persistent Identifierhttp://hdl.handle.net/10722/49096
ISSN
2015 Impact Factor: 4.085
2015 SCImago Journal Rankings: 1.780
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, TMen_HK
dc.contributor.authorHo, SKNen_HK
dc.contributor.authorLai, CLen_HK
dc.contributor.authorCheng, IKPen_HK
dc.contributor.authorLai, KNen_HK
dc.date.accessioned2008-06-12T06:34:20Z-
dc.date.available2008-06-12T06:34:20Z-
dc.date.issued1999en_HK
dc.identifier.citationNephrology Dialysis Transplantation, 1999, v. 14 n. 3, p. 717-722en_HK
dc.identifier.issn0931-0509en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49096-
dc.description.abstractBackground. The pathogenetic mechanisms of chronic hepatitis C virus (HCV) infection in renal allograft recipients are not well established. This study aimed to examine the relationship between altered immune status and HCV-related liver disease, by determining the changes in peripheral blood lymphocyte and natural killer (NK) cell subsets in these subjects. Methods. Peripheral blood lymphocyte, NK cell and activation markers were detected by flow cytometry in renal allograft recipients with (TpC+) or without (TpC-) HCV infection, and compared with age- and sex-matched patients with post-transfusional chronic HCV infection (TfC+) and healthy controls. Results. CD19+ cells were reduced in renal allograft recipients compared with controls. TpC+ subjects had increased CD3+CD8+ cells compared with controls, and increased CD3+DR+ cells but reduced CD4+CD38+ and CD3-CD16/56+ cells compared with controls as well as TfC+ patients. TfC+ patients and controls had similar numbers and proportions for the lymphocyte subsets and NK cells. Chronic liver disease in HCV-infected renal allograft recipients was associated with increased CD3+CD16/56+ cells but reduced CD4+CD38+ cells. Reduction of CD3-CD16/56+ cells was noted in TpC+ subjects without liver disease. Yet among post-transfusional (TfC+) subjects this was associated with chronic hepatitis. Conclusions. Peripheral blood suppressor/cytotoxic T lymphocytes are increased, whereas activated helper/inducer T lymphocytes and NK cells are reduced, in renal allograft recipients with HCV infection. Increased non-MHC-restricted cytotoxic T cells and reduced NK cells are associated with the presence or absence of liver disease respectively. These data suggest that immune mechanisms are important in the pathogenesis of chronic hepatitis C after renal transplantation.en_HK
dc.format.extent420 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://ndt.oxfordjournals.org/en_HK
dc.relation.ispartofNephrology Dialysis Transplantationen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsNephrology, Dialysis, Transplantation. Copyright © Oxford University Press.-
dc.subjectHepatitis Cen_HK
dc.subjectLymphocyteen_HK
dc.subjectNatural killer cellen_HK
dc.subjectRenal transplantationen_HK
dc.titleLymphocyte subsets in renal allograft recipients with chronic hepatitis C virus infectionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0931-0509&volume=14&issue=3&spage=717&epage=722&date=1999&atitle=Lymphocyte+subsets+in+renal+allograft+recipients+with+chronic+hepatitis+C+virus+infectionen_HK
dc.identifier.emailChan, TM: dtmchan@hku.hken_HK
dc.identifier.emailLai, CL: hrmelcl@hku.hken_HK
dc.identifier.emailLai, KN: knlai@hku.hken_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.identifier.authorityLai, CL=rp00314en_HK
dc.identifier.authorityLai, KN=rp00324en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1093/ndt/14.3.717en_HK
dc.identifier.pmid10193826-
dc.identifier.scopuseid_2-s2.0-0033045431en_HK
dc.identifier.hkuros41545-
dc.identifier.hkuros49753-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033045431&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue3en_HK
dc.identifier.spage717en_HK
dc.identifier.epage722en_HK
dc.identifier.isiWOS:000079192400038-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.scopusauthoridHo, SKN=36839065300en_HK
dc.identifier.scopusauthoridLai, CL=7403086396en_HK
dc.identifier.scopusauthoridCheng, IKP=7102537483en_HK
dc.identifier.scopusauthoridLai, KN=7402135706en_HK

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