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. 2019 Apr 15;10(5):332. doi: 10.1038/s41419-019-1565-6

Fig. 2. Knockdown of miR-142-3p improves the proliferation, apoptosis, and function of in vitro induced Tregs (iTregs) in an inflammatory environment (n = 3).

Fig. 2

Naive T cells were purified and induced as iTregs. iTregs were treated with a miR-142-3p inhibitor or mimic for 3 days on day 7. Interleukin-1β (IL-1β) (10 ng/ml) and IL-6 (10 ng/ml) (R&D Systems, Minneapolis, MN, USA) were added to the media on day 10. iTregs were harvested on day 11 for detection. a Forkhead box P3 (Foxp3) histogram of iTregs treated with inhibitor or mimic (gated on CD4+CD127− cells). Representative result. b Foxp3 expression of iTregs from each group. c Annexin V apoptosis detection using propidium iodide (PI) staining of iTregs treated with an inhibitor or mimic in a normal or inflammatory environment (gated on CD4+CD127− cells). Representative result. d %Annexin V+ PI− of iTregs from each group. e Ki67 histogram of iTregs treated with inhibitor or mimic in an inflammatory environment (gated on CD4+CD127− cells). Representative result. f Level of Ki67 expression after antagomir/agomir treatment. g Division index of CD8+ T cells mediated with anti-CD3 proliferation in vitro, ratio range 1:2 to 1:16 (iTreg:peripheral blood mononuclear cells) as detected using carboxyfluorescein succinimidyl ester dye dilution. Results are presented as mean ± standard error of the mean values (*P < 0.05 and **P < 0.01)