In particular, it has been shown that leukocyte IFN-γ production is reduced by WJ-MSCs14; TGF-β1, released by WJ-MSCs, inhibits T-lymphocyte activation and proliferation.30 Furthermore, WJ-MSCs downregulate many surface markers of monocyte-derived dendritic cells involved in inflammatory responses (i.e., CD1a, CD14, and the T costimulation complex CD86/CD80).31,32 For these reasons, the use of WJ-MSCs may also determine a low risk of a graft versus host disease development. This evidence concerns the gene CD86 and glycogen storage disease VI.