Figure 2
Figure 2. Phenotype of tumor-polarized macrophages from fibrosarcoma and ovarian carcinoma models. (Top panel) TAM phenotype from chemically induced fibrosarcoma model showing modulation of selected genes after LPS stimulation, compared with normal peritoneal macrophages. Red X indicates inhibition of NF-κB activation resulting from p50 homodimer overexpression. High or low expression is relative to that in peritoneal macrophages from non–tumor-bearing mice. (Bottom panel) Phenotype of bone marrow–derived macrophages or TAMs from ovarian carcinoma model on coculture with ID8 ovarian carcinoma cells. Red X indicates inhibition of STAT1 by IKKβ activation. (Right panel) Inhibition of NF-κB was done by means of targeted deletion of IKKβ (IKKβ−/−) or IKKβ-dn expression.

Phenotype of tumor-polarized macrophages from fibrosarcoma and ovarian carcinoma models. (Top panel) TAM phenotype from chemically induced fibrosarcoma model showing modulation of selected genes after LPS stimulation, compared with normal peritoneal macrophages. Red X indicates inhibition of NF-κB activation resulting from p50 homodimer overexpression. High or low expression is relative to that in peritoneal macrophages from non–tumor-bearing mice. (Bottom panel) Phenotype of bone marrow–derived macrophages or TAMs from ovarian carcinoma model on coculture with ID8 ovarian carcinoma cells. Red X indicates inhibition of STAT1 by IKKβ activation. (Right panel) Inhibition of NF-κB was done by means of targeted deletion of IKKβ (IKKβ−/−) or IKKβ-dn expression.

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