Allogeneic hematopoietic stem-cell transplantation (HSCT) remains one of the only curative therapies for acute leukemias, myelodysplasia and high-risk lymphoproliferative disorders. The efficacy of HSCT is thought to be largely driven by a powerful immunologic effect termed the graft-versus-tumor (GVT) effect mediated by the donor graft. In recent years, it has become apparent that relapse remains the chief complication of transplantation while non-relapse mortality has been vastly reduced by improved infection control and supportive measures. While GVT is thought to be primarily mediated by T-lymphocytes derived from the donor graft, NK cells, macrophages and other cellular and humoral components of the immune system are progressively being recognized as potential mediators. With a better understanding of the immunobiology of GVT, various strategies are being developed to augment the GVT effect, both peri-transplant and post-transplant with the ultimate goal of relapse prevention and more rational treatment strategies for tackling post-transplant relapse thought to be mediated by immune escape phenomena.
This collection will be focused on understanding the immunobiology of GVT and methods to augment it. We will include both pre-clinical strategies, those which have successfully been translated as well as strategies to modulate the post-transplant immune milieu.
All scientists and researchers interested in this Research Topic are invited to submit their work in the form of Original Research, Review, Mini-Review, and Perspective articles, offering new insights within the graft-versus-tumor effect perspective. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
1.Immunobiology of the graft-versus tumor effect in allogeneic transplantation;
2. Graft versus leukemia effect: T-cells ;
3.Graft-versus leukemia effect: NK cells;
4. Graft versus leukemia effect: The innate immune system;
5.Graft manipulation to augment GVL;
6.Checkpoint inhibition and GVL;
7.Novel strategies to augment GVT (pre-clinical and early translation);
8.Mutationally targeted strategies that augment GVT;
9. GVL and graft -versus-host-disease (GVHD):The yin and yang;
10.Immune escape mechanisms driving relapse post-transplantation.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation are considered out of scope of this section.
Topic Editor Dr. John Koreth is on the advisory boards of Cugene and Therakos (mallinckrodt), and consults for Equillium, Gentibo, Cue Biopharma, Biolojic Design, and TR1x. He also provides research support to Amgen, Clinigen, BMS, Miltenyi Biotec, Regeneron, Equillium, and legal support to Abbvie. Topic Editor Dr. Robert Zeiser provides consultancy to Novartis, Incyte, MNK, and Sanofi. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Allogeneic hematopoietic stem-cell transplantation (HSCT) remains one of the only curative therapies for acute leukemias, myelodysplasia and high-risk lymphoproliferative disorders. The efficacy of HSCT is thought to be largely driven by a powerful immunologic effect termed the graft-versus-tumor (GVT) effect mediated by the donor graft. In recent years, it has become apparent that relapse remains the chief complication of transplantation while non-relapse mortality has been vastly reduced by improved infection control and supportive measures. While GVT is thought to be primarily mediated by T-lymphocytes derived from the donor graft, NK cells, macrophages and other cellular and humoral components of the immune system are progressively being recognized as potential mediators. With a better understanding of the immunobiology of GVT, various strategies are being developed to augment the GVT effect, both peri-transplant and post-transplant with the ultimate goal of relapse prevention and more rational treatment strategies for tackling post-transplant relapse thought to be mediated by immune escape phenomena.
This collection will be focused on understanding the immunobiology of GVT and methods to augment it. We will include both pre-clinical strategies, those which have successfully been translated as well as strategies to modulate the post-transplant immune milieu.
All scientists and researchers interested in this Research Topic are invited to submit their work in the form of Original Research, Review, Mini-Review, and Perspective articles, offering new insights within the graft-versus-tumor effect perspective. We welcome manuscripts focusing on, but not limited to, the following sub-topics:
1.Immunobiology of the graft-versus tumor effect in allogeneic transplantation;
2. Graft versus leukemia effect: T-cells ;
3.Graft-versus leukemia effect: NK cells;
4. Graft versus leukemia effect: The innate immune system;
5.Graft manipulation to augment GVL;
6.Checkpoint inhibition and GVL;
7.Novel strategies to augment GVT (pre-clinical and early translation);
8.Mutationally targeted strategies that augment GVT;
9. GVL and graft -versus-host-disease (GVHD):The yin and yang;
10.Immune escape mechanisms driving relapse post-transplantation.
Manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by robust and relevant validation are considered out of scope of this section.
Topic Editor Dr. John Koreth is on the advisory boards of Cugene and Therakos (mallinckrodt), and consults for Equillium, Gentibo, Cue Biopharma, Biolojic Design, and TR1x. He also provides research support to Amgen, Clinigen, BMS, Miltenyi Biotec, Regeneron, Equillium, and legal support to Abbvie. Topic Editor Dr. Robert Zeiser provides consultancy to Novartis, Incyte, MNK, and Sanofi. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
