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- W2148291723 abstract "CD20 has been proposed as a novel suicide gene system for the treatment of graft-versus-host disease (GVHD), a fatal complication of allogeneic bone marrow transplantation: indeed expression of the human non-immunogenic exogenous CD20 protein allows positive immunoselection of transduced cells as well as their killing in vitro with rituximab. Lentiviral vectors are promising tools in the field of gene therapy. We therefore searched for a lentivector giving good efficiency of transduction of human T lymphocytes activated by the sole addition of interleukin (IL)-2 and high expression levels of the CD20 transgene.The T cell line CEM and peripheral T lymphocytes activated by phytohemagglutinin (PHA) and/or IL-2 were transduced with two different vectors carrying the CD20 transgene driven by either the phosphoglycerate kinase (PGK) or elongation factor 1alpha (EF1alpha) promoter, and using different multiplicities of infection (MOIs).Both the PGK- and EF1alpha-CD20 vectors allowed efficient transduction of the CEM cell line and PHA-activated T cells, reaching 99 and 90% in the different targets, respectively. However EF1alpha-CD20 led to much higher expression levels of the transgene (mean fluorescence intensity 588-618 compared to 53 for PGK-CD20). Furthermore lymphocytes activated with IL-2 alone could be efficiently transduced with EF1alpha-CD20, reaching 10-25% positivity for CD20 (mean fluorescence intensity 409-424), allowing adequate immunoselection and strong complement-mediated lysis.EF1alpha-CD20 may represent a good candidate vector for gene therapy with the CD20 suicide system in the setting of allogeneic bone marrow transplants." @default.
- W2148291723 created "2016-06-24" @default.
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- W2148291723 creator A5018208681 @default.
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- W2148291723 date "2004-01-01" @default.
- W2148291723 modified "2023-10-18" @default.
- W2148291723 title "Elongation factor 1 (EF1alpha) promoter in a lentiviral backbone improves expression of the CD20 suicide gene in primary T lymphocytes allowing efficient rituximab-mediated lysis." @default.
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