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. 2016 Mar 22;7:101. doi: 10.3389/fimmu.2016.00101

Figure 3.

Figure 3

Positive feedback from IL-18 induces IL-18R. PBMCs were stimulated for 6 or 18 h in vitro and changes in NK cell surface expression of IL-18Rα was measured in response to Med (medium alone), IL-2, IL-12, IL-15, IL-18, or IL-21. Representative flow cytometry plots show gating of CD3+ T cells, CD3−CD56+ NK cells, and surface expression of IL-18Rα on unstimulated T cells and NK cells for IL-18Rα-FITC [N.B. as used in (D); IL-18Rα-PE used in (B,C)] (A). IL-18Rα expression on NK cells was measured after stimulation with Med, IL-2, IL-12, IL-15, IL-18, or IL-21 (concentrations per milliliter as labeled) for 6 (B) or 18 h (C) (n = 7–11 data from one to two experiments). Concentrations in boxes indicate those used in following graphs. IL-18Rα expression on NK cells was also measured after stimulation with a titration of IL-2 (0, 5, and 50 ng/ml) in combination with IL-12 (12.5 pg/ml), IL-15 (0.75 ng/ml), and/or IL-18 (10 ng/ml) after 18 h (D) (n = 8, data from two experiments). Box plots show the 5th to 95th percentile range. Data were analyzed using paired Wilcoxon signed-rank tests [(B–D) no lines; compared to Med] or ANOVA tests for linear trend for trend analysis across increasing cytokine concentrations including Med [(B–D), uncapped lines]. ****p < 0.0001, ***p < 0.001, **p < 0.01, *p < 0.05.