Figure 2

Activation of immune cell subsets in human PBMCs (Donor I) in response to TLR7/8 agonist stimulation. CD3-/CD56 + cells were gated as NK cells. Percentage of NK cells positive for the different markers are plotted on bar graphs. NK cells were then gated for (A) the activation marker CD69; all compounds showed significant improvement in CD69 expression when compared with antibody treatment (P < 0.0001). (B) the degranulation marker CD107a; all compounds other than 563 showed significant improvement in CD107a expression when compared with antibody treatment (P < 0.0001) and (C) the cytokine IFN-γ; all compounds other than 571 showed significant improvement in IFN-γ expression when compared with antibody treatment (P < 0.0001). CD8 and CD4 T cells were gated as CD3⁺/CD8⁺ and CD3⁺/CD4⁺, respectively. (D) CD8 T cells were then gated for the activation marker CD69; all compounds except 571 showed significant improvement in CD69 expression when compared with antibody treatment (P < 0.0001). (E) CD4 T cells were then gated for the activation marker CD69; all compounds other than 571 showed significant improvement in CD69 expression when compared with antibody treatment (P < 0.0001). All samples other than ‘PBMC Only’ contained A549 (target) cells. All samples other than ‘PBMC Only’ and ‘PBMC + A549’ contained cetuximab (200 nM). Statistical significance was measured by two-way ANOVA with multiple comparisons.