Figure 6.

Graphic overview of the functional articulation between the number of KIR ligands and main NK cell subsets in modulating rituximab-dependent NK ADCC responses. A sizable KIR ligand environment favors a higher frequency of inefficient KIR⁻ NK cells and numerous functional KIR/HLA inhibitions of educated KIR⁺ NK cells. By contrast, a low number of KIR ligands favor higher frequency of uneducated and educated NK cells that harbor a better rituximab-dependent ADCC than KIR⁻ NK cells