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. 2008 May 22;118(6):2269–2280. doi: 10.1172/JCI34610

Figure 7. IFN-γ in CD-CM promotes IL-23–hyperproducing proinflammatory macrophage differentiation.

Figure 7

(A) Quantification of IFN-γ and IL-6 in LPMC-CM. Data are shown as mean ± SEM from 3 individual normal controls and 4 individual patients with IBD used for macrophage differentiation experiments. (B) Flow cytometry for the surface phenotypes of IFN-γ–induced in vitro–differentiated macrophages. The shaded histogram shows the profiles of the indicated Ab staining and the open histogram shows staining with isotype controls. (C) Production of IL-12/IL-23p40 and IL-23 by bacteria-stimulated macrophages differentiated with or without IFN-γ. Data represent mean ± SEM from 3 independent experiments. (D) Effect of IFN-γ signal blocking using anti–IFN-γ Ab (α-IFNγ Ab) (1 μg/ml) combination with anti–IFN-γ receptor 1 Ab (α-IFNγR Ab) (10 μg/ml) or same amount of those isotype controls (mouse IgG; mouse IgG2A for α-IFNγ Ab, and mouse IgG1 for α-IFNγR Ab) from CD-CM on macrophage differentiation. Statistical analysis was performed using paired t test. Data represent mean ± SEM from 5 independent experiments. *P < 0.05 compared with controls.