Fig. 6

NKG2A-deficient mice display minor defects in NK-cell activity. a Poly(I:C)-primed splenocytes from the indicated mice were stimulated with plate-coated anti-NKR-P1C. Percentages of IFN-γ⁺ gated CD3⁻NKp46⁺ NK cells were analysed. b, c Licensing ratio of NKG2A for stimulation with plate-coated anti-NKR-P1C (b) or PMA and ionomycin (c). Licensing ratio is relative production of IFN-γ by NKG2A⁺ cells within gated CD3⁻NKp46⁺ NK cells comparing to NKG2A⁻ cells within gated NK cells from indicated mice. d Flow cytometry analysis of expression of the indicated receptors on splenic CD3⁻NKp46⁺ NK cells from WT (red line) and Klrc1^−/− (blue line) mice (shown as NKG2A KO mice). e Poly(I:C)-primed splenocytes from the indicated mice were stimulated with tumour target cells. Percentages of IFN-γ⁺ gated CD3⁻NKp46⁺ NK cells were analysed. f In vivo rejection of β2M-deficient splenocytes (similar to Fig. 3a). g In vivo rejection of β2M-deficient splenocytes (similar to Fig. 3d). Each symbol represents an individual mouse. Data shown represent two (f, g) or at least three (a–c, e) independent experiments. Mean ± SD is shown. *p < 0.05, **p < 0.01, ***p < 0.001 and ****p < 0.0001. Unpaired Student’s t-tests (two-tailed) was used to calculate these values. Source data are provided as a Source Data file