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. 2018 Nov 20;9:2676. doi: 10.3389/fimmu.2018.02676

Figure 4.

Figure 4

IL-10 signaling contributes to reduced LPS-induced pro-inflammatory cytokine production by IVIg-activated monocytes. In (A) monocytes from healthy control participants were left untreated (C) or stimulated with LPS (100 ng/ml), recombinant human IL-10 (rhIL-10; 400 pg/ml) or [rhIL-10 (400 pg/ml) + LPS (100 ng/ml)] for 24 h. Clarified cell supernatants were assayed for (A) IL-12/23p40, IL-6, and TNF. In (B,C) monocytes from healthy control participants were untreated (–) or pre-treated for 1 h with an IgG isotype control (IgG; 5 μg/ml) or an IL-10 receptor (IL-10R) blocking antibody (5 μg/ml). Cells were then stimulated with LPS (100 ng/ml) or [IVIg (5 mg/ml) + LPS (100 ng/ml)] for 24 h. Clarified cell supernatants were assayed for (B) IL-10, (C) IL-12/23p40, IL-6, and TNF. Data are mean ± SEM from n = 12 (A) or 8 (B,C) participants performed as independent experiments, assayed in duplicate. *p < 0.05 and **p < 0.01, and ***p < 0.001 for the comparisons indicated. Statistical analyses were performed using a non-parametric paired t-test in (A) and a repeated measures one-way ANOVA with Dunn's multiple comparisons correction in (B,C).