Fig. 1.

Loss of host IFNAR1 increases tumorigenesis and impairs host antitumor immunity. 1 × 10⁵ EO771.LMB cells were injected into the fourth mammary fat pad (IMFP) of wild type (WT) and Ifnar^−/− C57BL/6 mice (in which host IFNAR1 is deleted) at day 0 and subsequent alterations to circulating and primary tumor cells assessed. Peripheral blood (PB) was taken at day 7 for FACS analysis and for intracellular staining (ICS) of monocytes was performed at endpoint. Primary tumor a volume (mm³) from WT (n = 4); Ifnar^−/− (n = 5) mice and b weights (mg) of WT (n = 7); Ifnar^−/− (n = 6) mice at experimental endpoint. Flow cytometric analysis of PB c NK (NK1.1⁺) cell and d CD69⁺ NK cell frequency (%); WT (n = 7); Ifnar^−/− (n = 6) e Absolute number (cell #) of primary tumor NK cells (n = 5/group). Flow cytometric analysis of primary tumor (n = 5/group) f CD69⁺ and g IFNγ⁺ NK cell frequency (%) (h representative flow cytometry plots shown), i NK cell IFNAR1 expression and j mCherry⁺ EO771.LMB Rae-1 expression, represented as MFI (mean fluorescence intensity). Flow cytometric analysis of primary tumor (n = 5/group) k. CD4⁺ T cells IFNAR1 expression, l CD4⁺ IFNγ⁺ T cells, m CD8⁺ T cells IFNAR1 expression and n CD8⁺ IFNγ⁺ T cells, represented as frequency (%). p values * < 0.05, ** < 0.005, *** < 0.0005. **** < 0.0001 determined by Student’s t test. Errors bars, SEM