MHC-I engagement selectively inhibits cytotoxicity on activated human primary NK cells triggered by CD16, NKp46 or 2B4 but not by NKG2D activating receptors.

<p>(<b>A</b>) Phenotype of activated but quiescent polyclonal NK cells. Filled histograms represent isotype control and open histograms represent surface receptor stained cells. Numbers are percentages of positive cells in each panel. Data show one representative donor out of six tested in this study. (<b>B</b>) Purified quiescent NK cells were co-cultured with ⁵¹Cr-P815 cells at 2∶1 and 5∶1 E/T ratios in the presence of mAb IgG2a isotype control, anti-MHC-I or anti-NKG2A (<b>a</b>), or against KAR (CD16 undiluted (<b>b</b>), CD16 diluted 1/5 (<b>c</b>), NKG2D (<b>d</b>), NKp46 (<b>e</b>) and 2B4 (<b>f</b>)), plus control Ig, anti-MHC-I or anti-NKG2A mAb. One representative donor (n = 6) is shown. (<b>C</b>) Inhibition percentages (mean ±SD) for each inhibitory receptor in all performed assays. Statistically significant difference comparing MHC-I <i>versus</i> NKG2A inhibitory effect is presented, *p = 0.034. (D) <b>MHC-I engagement selectively inhibits cytotoxicity on activated human T cells triggered by anti-CD3 activating receptor.</b> Purified activated T cells were co-cultured with P815 cells at 5∶1 and 15∶1 E/T ratios in the presence of mAb against CD3 plus control IgG2a, CD33 (WM53) or MHC-I (W6/32) mAb. One representative donor (n = 5) is shown.