Expression and biological function of programmed death ligands in human placenta mesenchymal stem cells

Expression and biological function of programmed death ligands in human placenta mesenchymal stem cells
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人胎盘间充质干细胞程序性死亡配体的表达及生物学功能

DOI:
10.1002/cbin.10024
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发表时间:
2013-02-01
影响因子:
3.9
通讯作者:
Luan, Xiying
Luan, Xiying
中科院分区:
生物学4区
文献类型:
--
作者:
Wang, Guoyan;Zhang, Siying;Luan, Xiying

文献摘要

被引文献

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间充质干细胞(MSCs)具有自我更新、多向分化和免疫抑制能力,在组织再生中发挥着重要作用。骨髓间充质干细胞可从脐带、脐血、胎盘等多种组织中分离出来。人胎盘间充质干细胞(HPMSCs)具有比人骨髓MSCs更强的免疫抑制特性,如抑制T细胞的激活和增殖的能力。我们研究了程序性死亡配体1和2(PDL1和PDL2)在hPMSC黏附、迁移和免疫抑制中的作用。HPMSCs高表达PDL1和PDL2。通过siRNA敲除PDL1和/或PDL2可增加hPMSC的黏附,但显著减少迁移。HPMSCs上表达的PDL1和PDL2通过阻断细胞周期抑制T细胞的增殖。然而,敲除hPMSCs中的PDL1和/或PDL2对CD69的表达没有影响,CD69是一种存在于CD4(+)和CD8(+)T细胞亚群上的T细胞早期激活标记。综上所述,负向共刺激因子PDL1和PDL2在hPMSCs的黏附、迁移和免疫抑制中起作用。这些发现可能有助于hPMSCs在临床细胞中的潜在应用。
Mesenchymal stem cells (MSCs) play important roles in tissue regeneration due to their self-renewal, multilineage differentiation and immunosuppression abilities. MSCs can be isolated from various kinds of tissue, such as umbilical cord, cord blood and placenta. Human placenta mesenchymal stem cells (hPMSCs) possess stronger immunosuppressive properties, such as the ability to inhibit T-cell activation and proliferation, than human bone marrow MSCs. We have investigated that the roles of the programmed death ligands 1 and 2 (PDL1 and PDL2) in hPMSC adhesion, migration and immunosuppression were investigated. PDL1 and PDL2 were highly expressed by hPMSCs. Knockdown of PDL1 and/or PDL2 by siRNA increased hPMSC adhesion, but greatly decreasing migration. PDL1 and PDL2 expressed on hPMSCs inhibited T-cell proliferation by arresting the cell cycle. Knockdown of PDL1 and/or PDL2 in hPMSCs, however, had no effect on the expression of CD69, a T-cell early activation marker found on both CD4(+) and CD8(+) T-cell subsets. In summary, the roles of the negative co-stimulators PDL1 and PDL2 is on the adhesion, migration and immunosuppression of hPMSCs. These findings may be useful regarding the potential use of hPMSCs in clinical cell.