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Article: Targeting of interleukin-10 is superior to cytotoxic T-lymphocyte associated antigen 4 with human immunoglobulin G 1 for the prevention of chronic allograft deterioration in organ transplantation

TitleTargeting of interleukin-10 is superior to cytotoxic T-lymphocyte associated antigen 4 with human immunoglobulin G 1 for the prevention of chronic allograft deterioration in organ transplantation
Authors
KeywordsAdeno-associated viral vector
Chronic rejection
Gene therapy
Interleukin-10
Transplant arteriosclerosis
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/1099-498X
Citation
Journal Of Gene Medicine, 2008, v. 10 n. 12, p. 1315-1323 How to Cite?
AbstractBackground: Genetic manipulation of the allograft is an attractive approach to prevent the graft against chronic deterioration through stable expression of immunomodulatory or protective genes. However, the best strategy for prevention of chronic allograft deterioration remains unclear. Methods: The efficacies of adeno-associated viral vector-mediated stable expression of indoleamine 2,3-dioxygenase (IDO), cytotoxic T-lymphocyte associated antigen 4 with human immunoglobulin G 1 (CTLA4Ig) or interleukin-10 (IL-10) in the prevention of chronic allograft deterioration were compared in a rat heart transplantation model. Results: Transduction of grafts with IL-10 significantly prolonged allograft survival, whereas transduction of grafts with IDO did not improve graft survival compared to controls. Analysis of long-term survived heart allografts showed that both CTLA4Ig and IL-10 could significantly reduced the T cells and macrophage infiltration. However, stable expression of CTLA4Ig failed to prevent the development of transplant arteriosclerosis. By contrast, IL-10 suppressed the development of transplant arteriosclerosis effectively. The suppressive effects of IL-10 in preventing the development of chronic allograft deterioration were associated with lower transcript levels of transforming tumor growth factor beta 1 and macrophage migration inhibitory factor in the graft. In addition, higher transcript levels of heme oxygenase-1 were found in IL-10-transduced allograft. Conclusions: Targeting on IL-10 is superior to CTLA4Ig or IDO for the treatment of chronic allograft deterioration. Copyright © 2008 John Wiley & Sons, Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/59935
ISSN
2015 Impact Factor: 3.246
2015 SCImago Journal Rankings: 1.025
ISI Accession Number ID
Funding AgencyGrant Number
CRCG program of The University of Hong Kong
Faculty of Medicine, University of Regensburg.
Funding Information:

This work was supported by CRCG program of The University of Hong Kong and ReForm C program of the Faculty of Medicine, University of Regensburg.

References

 

DC FieldValueLanguage
dc.contributor.authorXu, Ten_HK
dc.contributor.authorHaering, Cen_HK
dc.contributor.authorLau, CKen_HK
dc.contributor.authorObed, Aen_HK
dc.contributor.authorMa, Jen_HK
dc.contributor.authorDoenecke, Aen_HK
dc.contributor.authorScherer, MNen_HK
dc.contributor.authorSchnitzbauer, AAen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorSchlitt, HJen_HK
dc.contributor.authorTsui, TYen_HK
dc.date.accessioned2010-05-31T04:00:27Z-
dc.date.available2010-05-31T04:00:27Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Gene Medicine, 2008, v. 10 n. 12, p. 1315-1323en_HK
dc.identifier.issn1099-498Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/59935-
dc.description.abstractBackground: Genetic manipulation of the allograft is an attractive approach to prevent the graft against chronic deterioration through stable expression of immunomodulatory or protective genes. However, the best strategy for prevention of chronic allograft deterioration remains unclear. Methods: The efficacies of adeno-associated viral vector-mediated stable expression of indoleamine 2,3-dioxygenase (IDO), cytotoxic T-lymphocyte associated antigen 4 with human immunoglobulin G 1 (CTLA4Ig) or interleukin-10 (IL-10) in the prevention of chronic allograft deterioration were compared in a rat heart transplantation model. Results: Transduction of grafts with IL-10 significantly prolonged allograft survival, whereas transduction of grafts with IDO did not improve graft survival compared to controls. Analysis of long-term survived heart allografts showed that both CTLA4Ig and IL-10 could significantly reduced the T cells and macrophage infiltration. However, stable expression of CTLA4Ig failed to prevent the development of transplant arteriosclerosis. By contrast, IL-10 suppressed the development of transplant arteriosclerosis effectively. The suppressive effects of IL-10 in preventing the development of chronic allograft deterioration were associated with lower transcript levels of transforming tumor growth factor beta 1 and macrophage migration inhibitory factor in the graft. In addition, higher transcript levels of heme oxygenase-1 were found in IL-10-transduced allograft. Conclusions: Targeting on IL-10 is superior to CTLA4Ig or IDO for the treatment of chronic allograft deterioration. Copyright © 2008 John Wiley & Sons, Ltd.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/1099-498Xen_HK
dc.relation.ispartofJournal of Gene Medicineen_HK
dc.rightsJournal of Gene Medicine. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectAdeno-associated viral vectoren_HK
dc.subjectChronic rejectionen_HK
dc.subjectGene therapyen_HK
dc.subjectInterleukin-10en_HK
dc.subjectTransplant arteriosclerosisen_HK
dc.titleTargeting of interleukin-10 is superior to cytotoxic T-lymphocyte associated antigen 4 with human immunoglobulin G 1 for the prevention of chronic allograft deterioration in organ transplantationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1099-498X&volume=10&issue=12&spage=1315&epage=1323&date=2008&atitle=Targeting+of+interleukin-10+is+superior+to+cytotoxic+T-lymphocyte+associated+antigen+4+with+human+immunoglobulin+G(1)+for+the+prevention+of+chronic+allograft+deterioration+in+organ+transplantationen_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jgm.1250en_HK
dc.identifier.pmid18816483-
dc.identifier.scopuseid_2-s2.0-58949097010en_HK
dc.identifier.hkuros153741en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58949097010&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume10en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1315en_HK
dc.identifier.epage1323en_HK
dc.identifier.isiWOS:000262004100005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXu, T=7401627167en_HK
dc.identifier.scopusauthoridHaering, C=36891922900en_HK
dc.identifier.scopusauthoridLau, CK=7401968442en_HK
dc.identifier.scopusauthoridObed, A=23009911000en_HK
dc.identifier.scopusauthoridMa, J=7406201578en_HK
dc.identifier.scopusauthoridDoenecke, A=8098869700en_HK
dc.identifier.scopusauthoridScherer, MN=7102940618en_HK
dc.identifier.scopusauthoridSchnitzbauer, AA=11640268000en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridSchlitt, HJ=7005572464en_HK
dc.identifier.scopusauthoridTsui, TY=7006622455en_HK

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