Objective   To investigate the effect of micro ribonucleic acid (miRNA)-155 on two subtypes of regulatory T cell (Treg): induced Treg (iTreg) and natural Treg (nTreg).

  Methods   Naïve T cells and nTreg were isolated from peripheral blood mononuclear cell(PBMC) of healthy donors by magnetic cell sorting. Cells were divided into 3 groups during culture, including control group(naïve T cells were cultured with the presence of interleukin-2), iTreg group(naïve T cells were cultured with the presence of interleukin-2 and transforming growth factor-β) and nTreg group(nTreg cells was cultured with interleukin-2). Each group was divided into 3 subgroups(none, scramble or miRNA-155 antagomir subgroup, 3 wells in each subgroup). Expression level of miRNA-155 gene of none subgroup in 3 groups was detected by low density chip analysis method. The levels of surface marker CD25, Foxp3, CD127 of each subgroup in 3 groups were detected by flow cytometry. The percentage of CD4⁺ CD25⁺Foxp3⁺SOCS1⁺ Treg and suppressive function of Treg of each subgroup in 3 groups were also detected by flow cytometry.

  Results   Compared with control group and iTreg group, the expression level of miRNA-155 was significantly lower and SOCS1 was significantly higher in nTreg group(all in P<0.05). After the addition of miRNA-155 antagomir, no significant change was observed in the important surface markers of Treg like Foxp3, CD25, CD127. Compared with control group and iTreg group, the expression of SOCS1 in nTreg group increased significantly (both in P<0.05). The expression level of miRNA-155 of none subgroup in iTreg group was lower. The expression of SOCS1 increased after the miRNA-155 was inhibited by antagomir(miRNA-155 antagomir subgroup). In iTreg group, the suppressive function of Treg in miRNA-155 antagomir subgroup was higher than that in none subgroup at the ratio of 1:8, 1:16 and 1:32(all in P<0.05).

  Conclusion   Antagonism of miRNA-155 in vitro has no significant effect on the suppression function of nTreg, but can increase the SOCS1 expression level and suppression in vitro of iTreg.