American Society of Hematology

Figure 3.

$Figure 3. Adaptive and canonical NK cells from PNH patients are functional. (A) PBMCs from CMV-seropositive healthy individuals (Ctrl, n = 5) or PNH patients (PNH, n = 10) were stimulated in the presence of IL-12 and IL-18. After 18 hours, canonical (NKG2C−FcεRγ+, filled bars, black for FLAER+ and red for FLAER− from the PNH patients) and adaptive (NKG2C+FcεRγ−, patterned, in PNH patients only FLAER− given lack of FLAER+ cells in this fraction) NK cells from controls and PNH patients were analyzed for intracellular IFN-γ expression. (B) Frequencies of adaptive and canonical NK cells showing degranulation (surface CD107a) and cytokine production (intracellular IFN-γ and tumor necrosis factor expression) after 6 hours of stimulation with P815 target cells and anti-CD16 monoclonal antibody (mAb). **P > .01, 1-way analysis of variance.$

Adaptive and canonical NK cells from PNH patients are functional. (A) PBMCs from CMV-seropositive healthy individuals (Ctrl, n = 5) or PNH patients (PNH, n = 10) were stimulated in the presence of IL-12 and IL-18. After 18 hours, canonical (NKG2C⁻FcεRγ⁺, filled bars, black for FLAER⁺ and red for FLAER⁻ from the PNH patients) and adaptive (NKG2C⁺FcεRγ⁻, patterned, in PNH patients only FLAER⁻ given lack of FLAER⁺ cells in this fraction) NK cells from controls and PNH patients were analyzed for intracellular IFN-γ expression. (B) Frequencies of adaptive and canonical NK cells showing degranulation (surface CD107a) and cytokine production (intracellular IFN-γ and tumor necrosis factor expression) after 6 hours of stimulation with P815 target cells and anti-CD16 monoclonal antibody (mAb). **P > .01, 1-way analysis of variance.

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