| First Author | Xiang Z | Year | 2014 |
| Journal | Cancer Cell | Volume | 26 |
| Issue | 4 | Pages | 565-76 |
| PubMed ID | 25220446 | Mgi Jnum | J:216988 |
| Mgi Id | MGI:5610109 | Doi | 10.1016/j.ccr.2014.07.026 |
| Citation | Xiang Z, et al. (2014) Targeted activation of human Vgamma9Vdelta2-T cells controls epstein-barr virus-induced B cell lymphoproliferative disease. Cancer Cell 26(4):565-76 |
| abstractText | Epstein-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 Vgamma9Vdelta2-T cells efficiently killed EBV-transformed autologous lymphoblastoid B cell lines (EBV-LCL) through gamma/delta-TCR and NKG2D receptor triggering and Fas and TRAIL engagement. By inoculation of EBV-LCL in Rag2(-/-)gammac(-/-) mice and humanized mice, we established lethal EBV-LPD with characteristics close to those of the human disease. Adoptive transfer of pamidronate-expanded Vgamma9Vdelta2-T cells alone effectively prevented EBV-LPD in Rag2(-/-)gammac(-/-) mice and induced EBV-LPD regression in EBV(+) tumor-bearing Rag2(-/-)gammac(-/-) mice. Pamidronate treatment inhibited EBV-LPD development in humanized mice through selective activation and expansion of Vgamma9Vdelta2-T cells. This study provides proof-of-principle for a therapeutic approach using pamidronate to control EBV-LPD through Vgamma9Vdelta2-T cell targeting. |
