Fig. 6: BCG-stimulated NK cells modulate adaptive immune responses in the lung.

a Schematic diagram showing treatment strategy for (a–h) and quantification of lung surface B16-F10-gp33 metastases at day 20 (n = 6 mice/group, representative of two independent experiments). b Quantification of CD44⁺ gp33-specific CD8⁺ T cells in the lung (n = 6 mice/group, from one experiment). c Splenocytes were isolated from mice treated as in (a) and their cytotoxicity against B16-F10-ZsGreenLuc cells tested in an in vitro assay (n = 6 mice/group, from one experiment). d IFN-γ expression by lung CD4⁺ and CD8⁺ T cells following ex vivo restimulation (n = 6 mice/group, from one experiment). e Absolute number and frequency of cDC1s in the lungs (n = 18 mice/group for PBS IV and BCG IV and n = 12 for BCG IV + NK depletion, pooled from three independent experiments). f CCL5 expression by lung NK cells at day 20 (n = 12 mice/group, pooled from two independent experiments). g CCL5 protein concentration in lung homogenates (n = 6 mice/group, from one experiment). h, Schematic diagram showing treatment strategy and quantification of ZsGreen expression in mLN cDC1s (n = 6 mice per group, representative of two independent experiments). P values were calculated using two-tailed unpaired Student’s t test at a 95 % CI (f) or one-way ANOVA with Bonferroni multiple-comparison test (a–e, g, h). Data is depicted as mean ± SEM. PBS phosphate-buffered saline, IV intravenous, IP intraperitoneal, NK natural killer, depl depletion, cDC1s type 1 conventional dendritic cells, mLN mediastinal lymph node, ZsG ZsGreen.