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. Author manuscript; available in PMC: 2019 Dec 18.
Published in final edited form as: Immunity. 2018 Dec 11;49(6):1148–1161.e7. doi: 10.1016/j.immuni.2018.09.024

Figure 6. Molecular targeting of the non-canonical NFkB pathway stimulates IL12-producing DCs.

Figure 6.

(A) Expression of non-canonical NFkB pathway components (illustrated on the left) across immune populations. (B) Intravital micrographs of a MC38 tumor in an IL-12p40 reporter mouse treated with AF647-aCD40 mAbs. Tumor cells (red), AF647-aCD40 (white), IL-12p40 (green), TAM (blue). Dashed yellow line highlights the location of an IL-12p40+ cell; ▽ show TAM overlay ing with aCD40 mAbs. (C) Left: Intravital micrographs of MC38 tumors in IL-12p40-eΓ FP reporter mice treated with aCD40 or AZD5582. Untreated mice were used as controls. Green, IFN-γ -eYFP expressing cells; red, tumor cells. Right: Fold change of IL-12p40+ cells in each group after 48 hours and compared to baseline. (D-E) Ex vivo flow cytometry analysis of MC38 tumors in IL-12p40 reporter mice treated or not 48 hprior with agonistic aCD40 mAbs. CD45+ F4/80+ TAMs (black) and CD45+ F4/80– CD11chi MHCIIhi DCs (red). (D) Fold change of IL-12p40+ cells normalized to untreated mice (E) MFI of IL-12 reporter signal from TAM or DC. Data are representative of at least two independent experiments. n.s. = not significant, * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, One way ANOVA with multiple comparisons. See also Figure S6.