间充质干细胞
银屑病
间质细胞
免疫学
CD3型
免疫系统
癌症研究
白细胞介素2受体
转化生长因子
干细胞
医学
生物
T细胞
细胞生物学
CD8型
作者
Juan‐Juan Jiao,Xincheng Zhao,Ying Wang,Nannan Liang,Juan Li,Xiaohong Yang,Jianxiao Xing,Ling Zhou,Junqin Li,Ruixia Hou,Xinhua Li,Kaiming Zhang
标识
DOI:10.1111/1346-8138.16490
摘要
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)-β 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-β receptor (TGF-βR) 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-β receptors and activation of TGF-β/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-β receptors.
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