Journal
NATURE MEDICINE
Volume 9, Issue 9, Pages 1144-1150Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm915
Keywords
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Funding
- NCI NIH HHS [R01S CA8006, CA65237, CA92225, P01-CA49605] Funding Source: Medline
- NHLBI NIH HHS [HL57443, HL58520] Funding Source: Medline
- NIAID NIH HHS [AI49903] Funding Source: Medline
- NIDDK NIH HHS [DK61925] Funding Source: Medline
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Mature donor T cells cause graft-versus-host disease (GVHD), but they are also the main mediators of the beneficial graft-versus-tumor (GVT) activity of allogeneic bone marrow transplantation. Suppression of GVHD with maintenance of GVT activity is a desirable outcome for clinical transplantation. We have previously shown that donor-derived CD4(+)CD25(+) regulatory T cells inhibit lethal GVHD after allogeneic bone marrow transplantation across major histocompatibility complex (MHC) class I and II barriers in mice. Here we demonstrate that in host mice with leukemia and lymphoma, CD4(+)CD25(+) regulatory T cells suppress the early expansion of alloreactive donor T cells, their interleukin-2-receptor (IL-2R) alpha-chain expression and their capacity to induce GVHD without abrogating their GVT effector function, mediated primarily by the perforin lysis pathway. Thus, CD4(+)CD25(+) T cells are potent regulatory cells that can separate GVHD from GVT activity mediated by conventional donor T cells.
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