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Conference Paper: Cross-sectional study on hepatitis B virus-specific CD4+ T cell immune response after liver transplantation

TitleCross-sectional study on hepatitis B virus-specific CD4+ T cell immune response after liver transplantation
Authors
Issue Date2006
PublisherWiley & Sons
Citation
The 2006 Joint International Congress of the International Liver Transplantation Society (ILTS), the European Liver and Intestinal Transplant Association (ELITA), and the Liver Intensive Care Group of Europe (LICAGE), Milan, Italy, 3 - 6 May 2006. In Liver Transplantation, 2006, v. 12 n. 5, p. C-101 Abstract no. 403 How to Cite?
AbstractBackground/Aims: Hepatitis B virus (HBV)-specific T cells play a critical role in controlling viralreplication and maintaining the protective immunity against HBV reinfection. In this study, wecharacterized HBV-specific CD4+ T cell-mediated immune response after liver transplantation forHBV-associated liver disease.Methods: The function and frequency of circulating HBV-specific CD4+ T cells were studied byproliferation and enzyme-linked immunospot assays in 40 recipients without evidence of HBVrecurrence at 1 year (n=29) or at 5 years (n=11) after liver transplantation, and in 6 recipients withrecurrent HBV infection.Results: T cell proliferation response to mitogen (phytohemagglutinin) and recall antigen (tetanustoxoid) were maintained in recipients at 1 and 5 years after transplantation, comparable to those ofpre-transplant patients and healthy subjects, however, HBV-specific CD4+ T cell proliferationresponse and frequency significantly declined to either undetectable or very low levels. In recipientswith HBV recurrence, despite immunosuppression, a significant HBV-specific CD4+ T cell responsewas detectable, but did not correlate with viral load, histology and levels of liver transaminases.Conclusions: HBV-specific CD4+ T cell immune responses may evanesce with clearance of viralantigens after liver transplantation, suggesting the necessity of retaining a long-term prophylactictreatment or developing new strategies to induce HBV-specific immunity for prevention of HBVrecurrence.Figure The median levels of T cell proliferation (a) and median frequencies of interferon (IFN)-γ-secreting T cells (b) in response to in vitro challenge with hepatitis B surface (HBsAg) and coreantigen (HBcAg) in 11 HBV-naïve and 23 HBV-immune healthy subjects, 29 HBV-infected patientsbefore liver transplantation (LT), 29 at 1 year post-LT, 11 at 5 years post-LT, as well as 6 recipientswith recurrent HBV infection. * Significantly lower than pre-LT and HBV immune controls, **significantly lower than HBV immune control (P < 0.05, Mann-Whitney U test). Dot lines indicatethe significant level of HBV-specific immune response.
Persistent Identifierhttp://hdl.handle.net/10722/108295
ISSN
2015 SCImago Journal Rankings: 1.763

 

DC FieldValueLanguage
dc.contributor.authorLuo, Yen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorCheung, CKYen_HK
dc.date.accessioned2010-09-26T00:33:39Z-
dc.date.available2010-09-26T00:33:39Z-
dc.date.issued2006en_HK
dc.identifier.citationThe 2006 Joint International Congress of the International Liver Transplantation Society (ILTS), the European Liver and Intestinal Transplant Association (ELITA), and the Liver Intensive Care Group of Europe (LICAGE), Milan, Italy, 3 - 6 May 2006. In Liver Transplantation, 2006, v. 12 n. 5, p. C-101 Abstract no. 403en_HK
dc.identifier.issn1527-6473-
dc.identifier.urihttp://hdl.handle.net/10722/108295-
dc.description.abstractBackground/Aims: Hepatitis B virus (HBV)-specific T cells play a critical role in controlling viralreplication and maintaining the protective immunity against HBV reinfection. In this study, wecharacterized HBV-specific CD4+ T cell-mediated immune response after liver transplantation forHBV-associated liver disease.Methods: The function and frequency of circulating HBV-specific CD4+ T cells were studied byproliferation and enzyme-linked immunospot assays in 40 recipients without evidence of HBVrecurrence at 1 year (n=29) or at 5 years (n=11) after liver transplantation, and in 6 recipients withrecurrent HBV infection.Results: T cell proliferation response to mitogen (phytohemagglutinin) and recall antigen (tetanustoxoid) were maintained in recipients at 1 and 5 years after transplantation, comparable to those ofpre-transplant patients and healthy subjects, however, HBV-specific CD4+ T cell proliferationresponse and frequency significantly declined to either undetectable or very low levels. In recipientswith HBV recurrence, despite immunosuppression, a significant HBV-specific CD4+ T cell responsewas detectable, but did not correlate with viral load, histology and levels of liver transaminases.Conclusions: HBV-specific CD4+ T cell immune responses may evanesce with clearance of viralantigens after liver transplantation, suggesting the necessity of retaining a long-term prophylactictreatment or developing new strategies to induce HBV-specific immunity for prevention of HBVrecurrence.Figure The median levels of T cell proliferation (a) and median frequencies of interferon (IFN)-γ-secreting T cells (b) in response to in vitro challenge with hepatitis B surface (HBsAg) and coreantigen (HBcAg) in 11 HBV-naïve and 23 HBV-immune healthy subjects, 29 HBV-infected patientsbefore liver transplantation (LT), 29 at 1 year post-LT, 11 at 5 years post-LT, as well as 6 recipientswith recurrent HBV infection. * Significantly lower than pre-LT and HBV immune controls, **significantly lower than HBV immune control (P < 0.05, Mann-Whitney U test). Dot lines indicatethe significant level of HBV-specific immune response.-
dc.languageengen_HK
dc.publisherWiley & Sons-
dc.relation.ispartofLiver Transplantationen_HK
dc.titleCross-sectional study on hepatitis B virus-specific CD4+ T cell immune response after liver transplantationen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailCheung, CKY: cindycky@HKUCC-COM.hku.hken_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/lt.20832-
dc.identifier.hkuros118379en_HK
dc.identifier.volume12en_HK
dc.identifier.spage101en_HK

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