Guoyan Wang and Siying Zhang contributed equally to this work.
Expression and biological function of programmed death ligands in human placenta mesenchymal stem cells†
Version of Record online: 2 JAN 2013
© 2013 International Federation for Cell Biology
Cell Biology International
Volume 37, Issue 2, pages 137–148, February 2013
How to Cite
Wang, G., Zhang, S., Wang, F., Li, G., Zhang, L. and Luan, X. (2013), Expression and biological function of programmed death ligands in human placenta mesenchymal stem cells. Cell Biology International, 37: 137–148. doi: 10.1002/cbin.10024
- Issue online: 21 JAN 2013
- Version of Record online: 2 JAN 2013
- Accepted manuscript online: 20 DEC 2012 10:24AM EST
- Manuscript Accepted: 26 NOV 2012
- Manuscript Received: 19 NOV 2012
- mesenchymal stem cells;
- programmed death ligand
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.