Fig. 3.

The ratio of strong to weak KIR-binding peptide determines the change in inhibition. (A) Stabilization of HLA-Cw*0102 on T2 cells in the absence or presence of 1 μM or 10 μM peptide. (B) Degranulation of CD3⁻CD56⁺CD158b⁺ NK cells in response to T2 cells alone or incubated with a single peptide or a combination of VAP-DA and VAP-FA at 1 μM or 10 μM final. (C) Fraction of degranulating CD3⁻CD56⁺CD158b⁺ NK cells in response to T2 cells incubated with VAP-FA alone or in combination with VAP-DA. The peptide mixes tested consisted of different ratios of VAP-FA and VAP-DA, from 10% VAP-FA/90% VAP-DA to 100% VAP-FA, and differing by 10%, to a final total peptide concentration of 1 μM or 10 μM. Data are normalized to the degranulation observed in response to T2 cells incubated with 10 μM VAP-DA and represent the means ± SEM of three independent experiments. Arrows indicate the 50% VAP-FA point. (D) shows a linear regression of the data from C plotted as the fraction of degranulating CD3⁻CD56⁺CD158b⁺ NK cells against the ratio of VAP-FA to VAP-DA in the peptide mix. (E) Regression analyses for the peptide titration of VAP-FA alone. The full line indicates a linear regression and the dashed line a one-phase decay nonlinear regression. Correlation coefficients for both analyses are shown.