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Article: Targeted Activation of Human Vγ9Vδ2-T Cells Controls Epstein-Barr Virus-Induced B Cell Lymphoproliferative Disease

TitleTargeted Activation of Human Vγ9Vδ2-T Cells Controls Epstein-Barr Virus-Induced B Cell Lymphoproliferative Disease
Authors
Issue Date2014
PublisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/ccell
Citation
Cancer Cell, 2014, v. 26 n. 4, p. 565-576 How to Cite?
AbstractEpstein-Barr virus-induced lymphoproliferative disease (EBV-LPD) after transplantation remains a serious and life-threatening complication. Herein we showed that the aminobisphosphonate pamidronate-expanded human Vγ9Vδ2-T cells efficiently killed EBV-transformed autologous lymphoblastoid B cell lines (EBV-LCL) through γ/δ-TCR and NKG2D receptor triggering and Fas and TRAIL engagement. By inoculation of EBV-LCL in Rag2-/-γc-/- mice and humanized mice, we established lethal EBV-LPD with characteristics close to those of the human disease. Adoptive transfer of pamidronate-expanded Vγ9Vδ2-T cells alone effectively prevented EBV-LPD in Rag2-/-γc-/- mice and induced EBV-LPD regression in EBV+ tumor-bearing Rag2-/-γc-/- mice. Pamidronate treatment inhibited EBV-LPD development in humanized mice through selective activation and expansion of Vγ9Vδ2-T cells. This study provides proof-of-principle for a therapeutic approach using pamidronate to control EBV-LPD through Vγ9Vδ2-T cell targeting. © 2014 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/205893
ISSN
2015 Impact Factor: 23.214
2015 SCImago Journal Rankings: 13.922
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorXIANG, Z-
dc.contributor.authorLiu, Y-
dc.contributor.authorZheng, J-
dc.contributor.authorLiu, M-
dc.contributor.authorLU, A-
dc.contributor.authorGAO, Y-
dc.contributor.authorHu, H-
dc.contributor.authorLam, KT-
dc.contributor.authorChan, GCF-
dc.contributor.authorYang, Y-
dc.contributor.authorChen, H-
dc.contributor.authorTsao, GSW-
dc.contributor.authorBonneville M, M-
dc.contributor.authorLau, YL-
dc.contributor.authorTu, W-
dc.date.accessioned2014-10-20T09:21:46Z-
dc.date.available2014-10-20T09:21:46Z-
dc.date.issued2014-
dc.identifier.citationCancer Cell, 2014, v. 26 n. 4, p. 565-576-
dc.identifier.issn1535-6108-
dc.identifier.urihttp://hdl.handle.net/10722/205893-
dc.description.abstractEpstein-Barr virus-induced lymphoproliferative disease (EBV-LPD) after transplantation remains a serious and life-threatening complication. Herein we showed that the aminobisphosphonate pamidronate-expanded human Vγ9Vδ2-T cells efficiently killed EBV-transformed autologous lymphoblastoid B cell lines (EBV-LCL) through γ/δ-TCR and NKG2D receptor triggering and Fas and TRAIL engagement. By inoculation of EBV-LCL in Rag2-/-γc-/- mice and humanized mice, we established lethal EBV-LPD with characteristics close to those of the human disease. Adoptive transfer of pamidronate-expanded Vγ9Vδ2-T cells alone effectively prevented EBV-LPD in Rag2-/-γc-/- mice and induced EBV-LPD regression in EBV+ tumor-bearing Rag2-/-γc-/- mice. Pamidronate treatment inhibited EBV-LPD development in humanized mice through selective activation and expansion of Vγ9Vδ2-T cells. This study provides proof-of-principle for a therapeutic approach using pamidronate to control EBV-LPD through Vγ9Vδ2-T cell targeting. © 2014 Elsevier Inc.-
dc.languageeng-
dc.publisherCell Press. The Journal's web site is located at http://www.elsevier.com/locate/ccell-
dc.relation.ispartofCancer Cell-
dc.titleTargeted Activation of Human Vγ9Vδ2-T Cells Controls Epstein-Barr Virus-Induced B Cell Lymphoproliferative Disease-
dc.typeArticle-
dc.identifier.emailLiu, Y: yinpingl@hku.hk-
dc.identifier.emailZheng, J: teddy629@hku.hk-
dc.identifier.emailLam, KT: ktlama@graduate.hku.hk-
dc.identifier.emailChan, GCF: gcfchan@hku.hk-
dc.identifier.emailChen, H: hlchen@hku.hk-
dc.identifier.emailTsao, GSW: gswtsao@hku.hk-
dc.identifier.emailLau, YL: lauylung@hku.hk-
dc.identifier.emailTu, W: wwtu@hku.hk-
dc.identifier.authorityLiu, Y=rp00269-
dc.identifier.authorityZheng, J=rp02004-
dc.identifier.authorityChan, GCF=rp00431-
dc.identifier.authorityChen, H=rp00383-
dc.identifier.authorityTsao, GSW=rp00399-
dc.identifier.authorityLau, YL=rp00361-
dc.identifier.authorityTu, W=rp00416-
dc.identifier.doi10.1016/j.ccr.2014.07.026-
dc.identifier.pmid25220446-
dc.identifier.scopuseid_2-s2.0-84907996988-
dc.identifier.hkuros241186-
dc.identifier.volume26-
dc.identifier.issue4-
dc.identifier.spage565-
dc.identifier.epage576-
dc.identifier.isiWOS:000343343800015-
dc.publisher.placeUnited States-

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