MDS derived BM-MSCs did not differ in the ability to inhibit DC maturation and differentiation as compared to their normal counterparts. However, MDS-derived BM-MSCs had decreased capacity than to inhibit DC endocytosis, to induce IL12 secretion and to suppress DC mediated T cell proliferation. These effects were partly attributed to TGFβ1 derived from patient MSCs. The effects of LR MSCs on the differentiation, maturation and function of DCs were weaker as compared to higher risk MDS. This evidence concerns the gene TGFB1 and myelodysplastic syndrome.