129 Systemic Immune Response in Burn Patients IL-13 and IL-17A (r > 0.7; p < 0.001) and between non-classicalmonocytes and IL-4 (r > 0.5; p < 0.001). In the first and second week, there were negative correlations between classical monocytes and IL-6, IL-8, MCP-1 and GRO-α (r between -0.4 and -0.7; p < 0.001). Immature neutrophils showed a strong positive correlation in the third week with IL-6, IL-8, IL-10, MCP-1 and MIP-3α and in the fourth week with MCP-1 (r > 0.8; p < 0.001). In the first 2 weeks after injury, there were only weak positive correlations between T cells and soluble mediators, but this pattern changed in week 3 and 4, where strong correlations were predominantly found between T cells and immune mediators. In week 3, CD4+ T cells and Tregs showed strong negative correlations with MIP-1β (r < -0.8; p < 0.001) and CCR4+CCR6¯ Tregs showed a strong positive correlation with TGF-β1 and TGF-β2 (r > 0.7; p < 0.001). Four weeks after injury, we observed positive correlations between CCR4¯CCR6+ CD4+ T cells and MIP-1α, GRO-α and IFN-γ (r > 0.8; p < 0.001) and strong negative correlations between CD4+ T cells and IL-4, IL-8, IL-12p40, IL-13, IL-17A, IFN-γ and TNF-α (r < -0.9; p < 0.001). Seemingly, in week 1–3 the presence of innate immune cells can be linked to pro-inflammatory cytokines, while in week 3–4 most pronounced correlations were found between CD4+ T cell subsets and specific mediators (Figure 7). Figure 7. Heatmap of correlation coefficients of immune cells and soluble mediators over time. Significant (p < 0.05) correlation coefficients (r) of immune cell counts and fold change of soluble mediators at: (A) Week 1 (n = 13 patients); (B) Week 2 (n = 15 patients); (C) Week 3 (n = 10 patients); (D) Week 4 (n = 5 patients) after burn injury. Correlations were measured by Pearson test and results are shown in gray (not significant), red (positive correlation) or blue (negative correlation). 4
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