Enhanced helper T-cell activity facilitating autoantibody-mediated platelet clearance and CTL-mediated platelet (Plt)/megakaryocyte (MK) destruction is involved in the cellular immunopathogenesis of ITP. DXM-modulated MDSCs (CD33⁺CD11b⁺HLA-DR^low) from in vitro cultures (peripheral blood mononuclear cells [PBMCs] supplemented with interleukin-6 [IL-6], granulocyte macrophage CSF [GM-CSF]) results in elevated levels of functional molecules (ARG, NO), upregulation of suppressive cytokines (IL-10, transforming growth factor-β [TGF-β]) and eventually inhibition of CD4⁺ T-cell proliferation as well as CTL-induced cytotoxicity. In an ITP murine model (splenocyte engraftment from immune CD61 knockout [KO] mice), transfer of DXM-modulated CD11b⁺Gr1⁺ MDSCs (bone marrow [BM] supplemented with IL-6, macrophage-CSF [M-CSF]) alleviated the thrombocytopenia in severe combined immunodeficient mice. Both DXM-modulated human MDSCs and posttransfer murine splenocytes show increased expression of Ets1.