Fig. 2
From: Integrin CD11b activation drives anti-tumor innate immunity
CD11b suppresses PDGF-BB-dependent neovascularization and tumor growth. a CD31, Desmin, NG2, Smooth muscle actin (SMA) and Dextran immunostaining of blood vessels in LLC tumors from WT (white bars) and Itgam−/− (blue bars) mice (n = 10). b Blood vessel density (vessels/field) and number of vessel branch points/field in LLC tumors from WT (white bars) and Itgam−/− (blue bars) animals (n = 10). c Percent CD31+/SMA+, CD31+/Desmin+, CD31+/NG2+ vessels in tumors from WT (white bars) and Itgam−/− (blue bars) (n = 5). d Ratio of extravascular to intravascular FITC-dextran in LLC tumors from WT (white bars) and Itgam−/− (blue bars) mice (n = 5). e, f Pdgfb and Vegfa e mRNA (n = 3) and f PDGF-BB protein expression (n = 12) in LLC tumors from WT (white bars) and Itgam−/− (blue bars) mice (n = 3). g Left, FITC-Isolectin staining of whole mount retinas from newborn WT (white bars) and Itgam−/− (blue bars) mice. Right, Percent neovascularization at P1, P4, and P9 retinas in WT (white bars) and Itgam-/- (blue bars) mice (n = 5). h Desmin (red) and CD31 (green) immunostaining of LLC tumors from Imatinib and vehicle-treated WT (white bars) and Itgam-/- (blue bars) mice. i Tumor weight, number of blood vessels/field and percent Desmin/CD31 vessels per field from h (n = 10). Bar on micrographs indicates 50 µm. Error bars indicate sem. “n” indicates biological replicates. p < 0.05 indicates statistical significance, as determined by Student’s t-test for b–g and by Anova with Tukey’s post-hoc testing for i. Source data are provided in Source Data file
