Abstract
Acute graft-versus-host disease (GVHD) is one of the main complications of allogeneic hematopoietic stem-cell transplantation (HSCT). Acute GVHD is thought to occur as a result of alloreactivity arising from mismatches in major or minor histocompatibility antigens between donor and recipient. The immunologic sequence of events leading to acute GVHD is initiated with the activation of antigen-presenting cells (APCs) and their presentation of host antigens to alloreactive donor lymphocytes in secondary lymphoid tissue. This is followed by activation, proliferation, and differentiation of these lymphocytes into T-helper type 1 (Th1) effector cells. These effector cells then migrate to host target tissues where direct cytotoxicity along with locally and systemically released cytokines result in end-organ damage (Figure 1). Traditionally, prophylactic and therapeutic strategies for GVHD have relied on generalized immunosuppression. Given the lack of specificity, these methods often resulted in infectious complications as well as possible disease relapse due to suppression of the potentially curative graft-versus-malignancy effect. Certainly, better targeted and more effective therapies for the prevention and treatment of acute GVHD are needed.
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