Normal mesenchymal stem cells can improve the abnormal function of T cells in psoriasis via upregulating transforming growth factor-beta receptor

Psoriasis, a chronic inflammatory skin disease, is a refractory disorder. Previous studies have shown that the imbalance of the T-helper (Th)17/regulatory T cells (Treg) results in the immune imbalance of T cells in psoriatic patients, and that mesenchymal stem cells display an immunosuppressive role by promoting the differentiation of T cells into Treg, leading to a reduction in the proportion of Th17/Treg. Utility of mesenchymal stem cells is becoming a new approach for the treatment of immune disorders. Following co-culture of dermal mesenchymal stromal cells (DMSC) and CD3(+) T cells with or without transforming growth factor (TGF)-beta receptor inhibitor, the biological function and relative signal pathway of CD3(+) T cells were assessed by flow cytometry, transwell, real-time polymerase chain reaction and western blotting, respectively. Normal DMSC were more potent than psoriatic DMSC in inhibition of CD3(+) T-cell proliferation, and stimulation of CD3(+) T-cell apoptosis than psoriasis DMSC. Moreover, normal DMSC decreased the ratio of Th17/Treg, while enhancing the immunosuppressive effect of Tregs on effector T cells. However, TGF-beta receptor (TGF-beta R) inhibitor attenuated the effect of normal DMSC on CD3(+) T cells and Th17/Treg ratio. Additionally, the normal DMSC were more potent than the psoriatic DMSC in increasing TGF-beta receptors and activation of TGF-beta/SMAD pathway in psoriatic CD3(+) T cells. In conclusion, normal DMSC can partially improve the biological function and immunosuppressive ability of psoriatic CD3(+) T cells, possibly via upregulating the TGF-beta receptors.