Fig. 6

Interleukin-10 (IL-10) was responsible for the inhibition of DC differentiation by induced pluripotent stem cell-mesenchymal stem cells (iPSC-MSCs). Immature dendritic cells (iDCs) were prepared as in Fig. 2a in the absence (a, top row second panel) or in the presence (a, top row third panel) of iPSC-MSCs or using a transwell chamber system (a, top row fourth panel) to separate the monocytes (Mo) and iPSC-MSCs, or with the administration of the supernatant of cultured iPSC-MSCs (a, bottom row first panel). In addition, anti-IL-10 antibody (a, bottom row second panel) or the PGE2 synthesis inhibitor NS-398 (a, bottom row fourth panel) was added to monocyte-iPSC-MSCs co-cultures. Recombinant IL-10 (rhIL-10) was administered to the iDC culture system (a, bottom row third panel). After 5 days, DCs were harvested and phenotypic analysis was performed. a A representative experiment showing the percentage of CD14- or CD1a-positive cells. b The role of cell-cell contact involved in the effects of iPSC-MSCs on DC differentiation (statistical analysis for the expression of CD14 and CD1a in monocytes or DCs). c The role of soluble factors involved in the effects of iPSC-MSCs on DC differentiation (statistical analysis of the expression of CD14 and CD1a in monocytes or DCs). d IL-10 levels in the culture supernatant of iPSC-MSCs co-cultured with CD14⁺ monocytes in the presence of GM-CSF and IL-4 for 0, 1, and 5 days. e Prostaglandin E2 (PGE2) levels in the supernatants between iPSC-MSCs cultured with or without iDCs. Our findings were confirmed using U-iPSC-MSCs and A-iPSC-MSCs. The results are expressed as the mean ± SD of the percentages of marker-positive cells obtained from the analysis of six independent experiments using U-iPSC-MSCs. **P < 0.01, ***P < 0.001. N.S not significant