Successful in vitro priming of EBV-specific CD8+ T cells endowed with strong cytotoxic function from T cells of EBV-seronegative children

Am J Transplant. 2006 Sep;6(9):2169-76. doi: 10.1111/j.1600-6143.2006.01429.x. Epub 2006 Jun 22.

Abstract

Epstein-Barr virus (EBV)-seronegative transplant recipients are at high risk of developing EBV-associated post-transplant lymphoproliferative disorder (PTLD), and would maximally benefit from an EBV-directed T-cell therapy for prevention or treatment of PTLD. So far, efforts to activate CD8+ EBV-specific cytotoxic T lymphocytes (CTL) endowed with high specific cytotoxicity from EBV-seronegative children have failed. We compared the CD8+ CTL priming efficiency of three different modified activation protocols, based on lymphoblastoid cell lines (LCL) stimulation potentially enhanced by either LCL presentation through dendritic cells, or selection of IFN-gamma+ cultured cells, or culture in the presence of rhIL-12 and rhIL-7, according to the standard protocol for reactivation of EBV-specific CTL. We found that only specific LCL stimulation in the presence of rhIL-12 and rhIL-7 was able to reproducibly expand EBV-specific CD8+ CTL endowed with strong cytotoxic activity from truly EBV-seronegative children. The lines thus activated, which included specificities toward EBV latent and lytic proteins, showed high percentage CD8+ T cells, with <10% naïve CD8+/CCR7+/CD45RA+ cells. Overall, the total number of CD8+ central memory cells, and of CCR7 T-cell effectors was comparable to that observed in healthy EBV-seropositive controls. In conclusion, it is feasible to activate EBV-specific CD8+ CTL with suitable characteristics for in vivo employment from EBV-seronegative children.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antibodies, Viral / blood*
  • Bone Marrow Transplantation / adverse effects*
  • CD8-Positive T-Lymphocytes / virology*
  • Child
  • Dendritic Cells / immunology
  • Dendritic Cells / metabolism
  • Female
  • Herpesvirus 4, Human / immunology*
  • Humans
  • Interferon-gamma / metabolism
  • Interleukin-12 / pharmacology
  • Interleukin-7 / pharmacology
  • Leukocytes, Mononuclear / virology
  • Lymphoproliferative Disorders / etiology
  • Male
  • Phenotype
  • Recombinant Proteins / pharmacology
  • T-Lymphocytes, Cytotoxic / virology*

Substances

  • Antibodies, Viral
  • Interleukin-7
  • Recombinant Proteins
  • Interleukin-12
  • Interferon-gamma