Fig 1: KIR2DL-1,-2/3 blockade reverses the functional hypoactivity of GBM-derived NK-cells. (a) Functional analysis of blood- and GBM-derived NK-cells: NK-cell responsiveness was assessed by cell surface mobilization of CD107a and IFN-? production following K562 stimulation of resting or IL-2 preactivated PBMC and TIL at an effector to target ratio of 10:1 for 4.5 h. Representative dot plots are shown illustrating the capacity of blood and tumor-derived CD3-CD56+ NK-cells to express CD107a, IFN-? or both CD107a and IFN-? after stimulation with K562-0 cells or culture medium alone (none). (b,c) The activity and cytolytic potential of glioblastoma-derived NK-cells after KIR2DL-1,-2/3 blockade were assessed. (b) Blocking experiments revealed that Lirilumab significantly inhibited the binding of CD158a and CD158b mAb to blood- and tumor-derived NK-cells at a concentration of 30 µg/ml (****p < 0.0001). (c) IL-2 preactivated PBMC and TIL from different glioblastoma patients (n = 5) were pre-incubated with a human IgG4 isotype control mAb or Lirilumab (30 µg/ml), cocultured with culture medium (none), IFN-? pretreated HLA-class I deficient K562 cells (K562-0) and HLA-C expressing K562 cells (K562-HLA-C) at an effector to target ratio of 10:1 for 4.5 h and then analyzed by flow cytometry. The frequencies of CD107a+, IFN-?+and CD107a+IFN-?+CD3-CD56+ NK-cells were determined. Mean values + /- SD are depicted. P values were calculated using the two-tailed Mann–Whitney test (*p < 0.05, **p < 0.01).
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