4 Bone Marrow Research Diﬀerentiation (−) DC Proliferation (−) B cell Apoptosis (−) DC TNF-α (+) TGF-β1 (+) IL-6 (−) − PD-1 − Na¨ıve and memory T cell + T cell IFN-γ CD3 + NK cell Proliferation (+) + − Prodiuction (−) PGE2 IL-2 PHA-stimulated lymphocyte CD25 CD38 CD69 PHA-stimulated lymphocyte MSC − CD4 MSC CD8 MSC Escape from alloreactive T cells HSC + Class II molecule GVHD (−) Figure 1: MSCs interact with immune cells, representing potential cellular therapy to enhance allogeneic hematopoietic engraftment and prevent GVHD. MSCs reduced the expression of activation markers CD25, CD38 and CD69 on PHA-stimulated lymphocytes, making allogeneic HSCs and MSCs escape from recognition of alloreactive T-cells. MSCs suppressed the proliferation of PHA-stimulated CD3+, CD4+ and CD8+ lymphocytes. MSCs inhibit na¨ıve and memory T-cell responses to their cognate antigens by the engagement of the inhibitory molecule PD-1. MSCs inhibit the proliferation of B-cells and the diﬀerentiation of mature DCs from HSCs. MSCs induce DC apoptosis by downregulate TNF-α and TGF-β1 levels and upregulated IL-6 levels. MSCs inhibit the IL-2-induced proliferation of NK cells by producing PGE2. IFN-γ can stimulate MSCs to exhibit induction of class II molecule expression to prevent GVHD. diverse T-cell responses including GVHD [93]. MSCs can inhibit the diﬀerentiation of mature DCs from HSCs by arresting them at the precursor stage, interfere with DC antigen presentation, prevent DC migration ability, and induce DC apoptosis by downregulate TNF-α and TGF-β1 levels and upregulated IL-6 levels [93–95]. IFN-γ, which is produced by donor T-cells in response to antigen recog- nition, displays natural cytolytic activity against the cells missing markers of self-MHC class I, serves as an initiating stimulus for MSC immunosuppressive activity in vivo [88]. This indicates that the exposure to concentrated amounts of IFN-γ of MSCs can stimulate MSCs to exhibit induction of class II molecule expression, to prevent GVHD and provide the basis for a new potential strategy in prevention of GVHD [87–89, 96]. There is also evidences that MSCs can inhibit the IL-2-induced proliferation of natural killer