Regulatory effects of IFN-γon the expression of PDL2 on human placenta mesenchymal stem cells (hPMSCs) and the hPMSCs-induced differentiation of peripheral blood CD8+IL-10+T cell subsets / 中华微生物学和免疫学杂志

ABSTRACT

Objective To investigate the regulatory effects of IFN-γon the expression of pro-grammed death ligand 2 (PDL2) on human placenta mesenchymal stem cells (hPMSCs) and the hPMSCs-induced differentiation of peripheral blood CD 8+IL-10+T cell subsets .Methods hPMSCs were isolated from mature human placenta by enzyme digestion .The expression of PDL2 on hPMSCs and the regulatory effects of IFN-γon PDL2 expression were detected by RT-PCR and flow cytometry ( FCM ) , respectively . Peripheral blood mononuclear cells (PBMCs) were isolated from healthy subjects by density gradient centrif-ugation.T cells were purified with sheep red blood cells .FCM was used to detect the ratios of CD 8+IL-10+T cell subsets in PHA or CD3/CD28 beads activated T cells in the presence of hPMSCs treated with Anti-PDL2 McAb or IFN-γ.Results PDL2 molecules were highly expressed on hPMSCs that could be further enhanced by IFN-γ.The results of FCM demonstrated that hPMSCs could induce the differentiation of CD 8+IL-10+T cell subsets .The ratios of CD8+IL-10+T cell population in T cells activated by different stimulators including PHA and CD3/CD28 beads were significantly increased in the presence of hPMSCs as compared with those without hPMSCs (P<0.01).In addition, the antibody blocking experiments indicated that PDL 2 McAb down-regulated the percentages of CD 8+IL-10+T cell subsets in PHA or CD 3/CD28 beads stimulated T cells in the presence of hPMSCs as compared with those of unblocked groups .CD8+IL-10+T cell subsets were up-regulated in IFN-γtreated hPMSCs groups as compared with those of untreated groups .Conclusion hPMSCs could induce the differentiation of peripheral blood T cells into CD 8+IL-10+T cell subsets , which was enhanced by PDL 2 expressed on hPMSCs .IFN-γcould promote the differentiation of CD 8+IL-10+T cell subsets induced by hPMSCs through up-regulating the expression of PDL2 on hPMSCs.