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Abstract
Using murine bone marrow transplant model systems, it has been demonstrated that the administration of exogenous regulatory T cells (Treg), either at the time of transplant or several days later as a delayed lymphocyte infusion, can effectively ameliorate the deleterious effects of graft-versus-host disease (GVHD) while preserving graft-versus-leukemia effects. Similarly, the question arises as to whether homeostatic proliferation of donor-derived Treg could potentially prevent the occurrence of GVHD if it were determined that these cells underwent sufficient homeostatic proliferation to generate the Treg:effector T cell ratios required to accomplish this effect.
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