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The biology of acute graft-versus-host disease (GVHD) must be considered in the context of a host that has been injured by the underlying disease, conditioning regimen, and infection. These factors result in an environment that supports and sustains the clinical syndrome of acute GVHD through induction of inflammatory mediators such as chemokines, adhesion molecules, cytokines, and cellular effectors. If this cycle can be interrupted, GVHD might be ameliorated. Thus we are studying novel regimens to control GVHD, through both cellular engineering and application of new immunosuppressants, including sirolimus and denileukin diftitox.A second related interest is to understand and harness the graft-versus-leukemia (GVL) effect. Previous efforts to control GVHD, such as T cell depletion, have resulted in loss of GVL effect. Inhibition of inflammatory cytokines may result in reductions in GVHD with sparing of GVL effect. Furthermore, we have shown that we can use GVL effect to induce remissions in relapsed patients, but at the risk of inducing GVHD. We are studying whether the limitations of T cell depletion can be overcome with the judicious use of donor lymphocytes preemptively administered after transplantation. We are also assessing whether GVL effect can be harnessed to allow a reduction in transplantation conditioning and its associated toxicity.
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FRONTIERS IN IMMUNOLOGY (2024): 1328858-1328858
Transplantation and Cellular Therapy (2024)
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