Fig. 6

Interaction of NKG2A/HLA-E drives the PI3K/AKT inhibition in exhausted NK cells (a, b) The expression of NKG2A (a) and p-AKT (b) on PB NK cells between HL-60 tumor bearing mice and negative control at day 15. c The Frequency and MFI of NKG2A on NK cells from different tumor burden mice. d The correlation of NKG2A and p-AKT expression on HL-60 tumor bearing mice PB NK cells. e Anti-HLA-E treated THP-1 target cells increased P-AKT of primary NK cells after 5 days coculture and then stimulated with PMA and ionomycin for different time point. f NKG2A KO NK92 cells increased the p-AKT expression when cocultured with THP-1 cells under different E:T ratio of 1:1 and 5:1. g Anti-NKG2A and anti-HLA-E were unable to rescue the dysfunction of NK cells induced by the PI3K-AKT inhibitor (N = 3)