Fig. 1
From: Integrin CD11b activation drives anti-tumor innate immunity
CD11b ligation promotes pro-inflammatory macrophage signaling. a–f Relative mRNA expression of pro- and anti-inflammatory cytokines in a bone marrow derived macrophages (BMDM) from WT (white bars) or Itgam−/− (cyan bars) mice (n = 2–8); b tumor associated macrophages (TAM) from WT (white bars) and Itgam−/− (cyan bars) mice bearing LLC lung carcinoma tumors (n = 2–4); c Itgam−/− and Itgam or non-silencing siRNA transfected macrophages (n = 2–4); inset: cell surface expression levels of CD11b in transfected macrophages; d WT macrophages in the presence of non-specific (IgG) or anti-CD11b antibodies (n = 3), e murine macrophages adherent to ICAM-1, VCAM-1 or BSA coated plates (Susp) (n = 3) and f human macrophages adherent to ICAM-1 or BSA coated plates (Susp) (n = 3). g Immunoblotting of phosphoSer536 and total p65 NFκB RelA in WT and Itgam−/− macrophages stimulated with IFNγ + LPS; graph depicts quantification of relative pSer536 expression in WT (white bars) and Itgam−/− (blue bars) BMDM. h, i LLC tumor growth in WT and Itgam-/- mice adoptively transferred with h bone marrow derived and i tumor derived WT or Itgam−/− macrophages. j Relative mRNA expression of cytokines in whole LLC tumors from WT (white bars) and Itgam−/− (cyan bars) mice (n = 3). k LLC lung (n = 17), B16 melanoma (n = 9) and autochthonous PyMT mammary (n = 10–14) tumor weight in WT (black dots) and Itgam−/− (cyan dots) mice. l Tumor weight and volume of LLC tumors grown in WT (black dots) versus Itgam I332G knockin mice (cyan dots) (n = 6–7). Error bars indicate sem. “n” indicates biological replicates. p < 0.05 indicates statistical significance determined by Student’s t-test for a–g and j. and by Anova with Tukey post-hoc testing for h, i, k, l. Source data are provided in Source Data file
