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. 2018 Aug 13;8:12079. doi: 10.1038/s41598-018-30621-4

Figure 4.

Figure 4

D18 or TNF synergised with IL2 in T regs proliferation. PBMC were treated for 48 hours with the treatment indicated. (a) For T cons, single treatment by IL2 induced 21% more Ki67 expression (n = 4, p = 0.036); TNF or D18 alone induced no significant regulation; the combination of TNF or D18 with IL2 induced no significant difference in the level of Ki67 compared to IL2 alone. For T regs, single treatment by IL2 induced significantly more Ki67 expression (49.3% more, n = 4 and p = 0.012); TNF or D18 alone induced no significant regulation of Ki67; the combination of TNF or D18 with IL2 induced significantly more Ki67 expression than IL2 itself (n = 4, p = 0.002 or p = 0.028 respectively). (b) A quarter of one million PBMCs were counted and analysed with a flow cytometer, in which none of the treatment significantly regulated the number of T cons. For T regs, IL2 treatment induced a 140% increase in cell numbers, the combination of TNF or D18 induced a further increase in cell numbers (57% more or 35% more respectively, n = 6, p = 0.008 or p = 0.007 respectively). (c) For T cons, only single treatment by TNF significantly up-regulated NFκB2 expression (n = 6, p = 0.007), IL2 or the combination of IL2 with TNF or D18 induced no significant regulation. For T regs, all of the single treatments by TNF, D18 or IL2 significantly up-regulated NFκB2 expression (n = 6, p = 0.005, p = 0.021 or p = 0.049 respectively); the combination of TNF or D18 with IL2 induced significantly more NFκB2 expression than IL2 alone (n = 6, p = 0.021 or p = 0.008 respectively). (*p < 0.05 compared to untreated; #p < 0.05 compared to IL2 treated.)