Figure 4.

Effects of UC-MSCs on T cell proliferation and cytokine production. (a) UC-MSCs inhibited PHA-induced T-cell proliferation in a dose-dependent fashion. T cells (1 × 105) were activated with PHA in the presence or absence of irradiated UC-MSCs in different ratio in 96-well plates. Inhibition of T cell proliferation was also found in the transwell system. All the data are expressed as the mean ± SD of more than three independent experiments. **P < 0.01, vs. the control. (b) Anti-TGF-β1, INDO and L-NAME restored T-cell proliferation. T cells (1 × 105) were activated with PHA in the presence or absence of irradiated UC-MSCs (2 × 104) in 96-well plates. The incorporation of (3H)-thymidine is shown by CPM. All the data are expressed as the mean ± SD of more than three independent experiments. **P < 0.01. (c) UC-MSCs suppressed T cells from producing pro-inflammatory cytokine TNF-α. T cells (1 × 106) from RA patients and UC-MSCs (5 × 104) were separated in the transwell system or cocultured in the cell-to-cell contact system in 24-well plates. After 72 hours, TNF-α in culture supernatants was determined. All the data are expressed as the mean ± SD of more than three independent experiments. ** P < 0.01, * P < 0.05 vs. the controls, respectively.

Liu et al. Arthritis Research & Therapy 2010 12:R210   doi:10.1186/ar3187
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