FOXP3 and myelodysplastic syndrome: Suppressive mechanisms of natural killer cells, T cells, FOXP3 + regulatory T cells, and myeloid-derived suppressor cells may impair T-cell function in patients with MDS [26] While immunosuppression (via T-cell depletion, antithymocyte globulin, and alemtuzumab) is an effective therapy for some patients with MDS, the exact mechanism remains unclear, and selection of patients who may benefit remains a challenge [7].