Abstract
Patients with myelodysplastic syndrome (MDS) have intrinsic, usually acquired genetic defects in their hematopoietic stem cells, but some others exhibit T-cell-mediated inhibition of hematopoiesis and good responses to immunosuppression. In these cases, MDS shares a similar pathophysiology with aplastic anemia (AA). Here, we review the evidence supporting a role of the immune system in the pathophysiology of MDS and the results of clinical trials of immunosuppressive agents.
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