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Adoptively transferred TRAIL^sup +^ T cells suppress GVHD and augment antitumor activity
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Adoptively transferred TRAIL^sup +^ T cells suppress GVHD and augment antitumor activity
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Journal Article
Adoptively transferred TRAIL^sup +^ T cells suppress GVHD and augment antitumor activity
2013
Overview
Current strategies to suppress graft-versus-host disease (GVHD) also compromise graft-versus-tumor (GVT) responses. Furthermore, most experimental strategies to separate GVHD and GVT responses merely spare GVT function without actually enhancing it. We have previously shown that endogenously expressed TNF-related apoptosis-inducing ligand (TRAIL) is required for optimal GVT activity against certain malignancies in recipients of allogeneic hematopoietic stem cell transplantation (allo-HSCT). In order to model a donor-derived cellular therapy, we genetically engineered T cells to overexpress TRAIL and adoptively transferred donor-type unsorted TRAIL^sup +^ T cells into mouse models of allo-HSCT. We found that murine TRAIL^sup +^ T cells induced apoptosis of alloreactive T cells, thereby reducing GVHD in a DR5-dependent manner. Furthermore, murine TRAIL^sup +^ T cells mediated enhanced in vitro and in vivo antilymphoma GVT response. Moreover, human TRAIL^sup +^ T cells mediated enhanced in vitro cytotoxicity against both human leukemia cell lines and against freshly isolated chronic lymphocytic leukemia (CLL) cells. Finally, as a model of off-the-shelf, donor-unrestricted antitumor cellular therapy, in vitro-generated TRAIL^sup +^ precursor T cells from third-party donors also mediated enhanced GVT response in the absence of GVHD. These data indicate that TRAIL-over-expressing donor T cells could potentially enhance the curative potential of allo-HSCT by increasing GVT response and suppressing GVHD. [PUBLICATION ABSTRACT]
Publisher
American Society for Clinical Investigation
