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[Preprint]. 2023 Sep 5:2023.09.01.555962. [Version 1] doi: 10.1101/2023.09.01.555962

Fig. 3. Educated NK cell subsets are more responsive to missing-self and NK cell activation can be abrogated by blockade of activating receptors.

Fig. 3.

PBMC from healthy donors (n=20) were cocultured with stimulators and profiled by CyTOF. a Subsets were defined by gating on CD56dim NK cells followed by combinatorial expression of educating inhibitory receptors, NKG2A, KIR3DL1, KIR3DL2, KIR2DL1/S1, KIR2DL2 and KIR2DL3 and the CD57 maturation marker. Percent CD107a+ when stimulated by K562 WT increases with NKG2A/KIR expression. b NKG2A+NKG2C− NK cells increased CD107a when stimulated by K562 WT and increase was depressed by stimulation with HLA-E+ K562. NKG2A–NKG2C+ NK cells increased CD107a when stimulated by K562 which was further increased by stimulation with HLA-E+ K562. c In individuals who expressed KIR3DL1 and class I HLA alleles that encode Bw4 (n=17), NKG2A–NKG2C–KIR3DL1sp NK cells increased CD107a in response to 4 allogeneic stimulator B cells and K562 but was relatively inhibited by stimulator 1 which uniquely expressed Bw4. d Percent CD107a+ for NKG2D+DNAM-1+ NK cells was decreased by blockade of NKG2D and DNAM-1. P value was calculated as one-way ANOVA as indicated and as 2-sided paired Student’s t-test; t-test p values were adjusted for multiple testing with Bonferroni correction and ns indicates p > 0.1.