A proposed model of regulation of DC destiny by MSCs. We propose that MSCs mediate their immunomodulatory effects by influencing DC fate. MSCs, via a critical cell-cell contact mechanism, not only drive imDCs or maDCs to escape their traditional destiny of apoptosis, but also induce them into a novel Ia^lowCD11b^hig regDC population, MSC-DCs, capable of suppressing lymphocyte activities through up-regulation of Jagged-2 and increasing secretion of IL-10 and TGF-β. Ia^low indicates a low-level expression of Ia molecules; CD11b^hig, a high level expression of CD11b.