Th type 17 (Th17) cells have been identified as a proinflammatory T-cell subset. Here, we investigated the regulation of human Th17 cells by fetal BM-derived mesenchymal stem cells (FBM-MSC). We cocultured. FBM-MSC with human PBMC or CD4(+) T cells from healthy donors. FBM-MSC significantly suppressed the proliferation of CD4(+) T cells stimulated by PHA and recombinant IL-2. Significantly higher levels of IL-17 were observed in FBM-MSC cocultured with either PBMC or CD4(+) T cells than that in PBMC cultured alone or CD4(+) T cells cultured alone. Flow cytometry analysis showed that the percentage of Th17 cells in coculture of FBM-MSC and CD4(+) T cells was significantly higher than that in CD4(+) T-cell cultured alone. FBM-MSC did not express IL-17 protein. Consistent with the augmentation of Th17 cells, significantly higher levels of IL-6 and IL-17 were observed in coculture of FBM-MSC and CD4(+) T cells than that in CD4(+) T-cell culture, while the levels of IL-23 were similar between FBM-MSC + PBMC coculture and PBMC alone, or FBM-MSC + CD4(+) T-cell and CD4(+) T-cell alone. The presence of FBM-MSC decreased the percentage of Th1 cells, but minimally affected the expansion of CD4(+)CD25(+) T cells. In conclusion, our data demonstrate for the first time that FBM-MSC promote the expansion of Th17 cells and decrease IFN-gamma-producing Th1 cells. These data suggest that IL-6 and IL-1, instead of IL-23, may be partly involved in the expansion of Th17 cells.