Skip to main content
. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: Clin Cancer Res. 2013 Feb 26;19(7):1858–1872. doi: 10.1158/1078-0432.CCR-12-2426

Figure 5.

Figure 5

Enhancement by cetuximab of NK-DC cross-talk is NKG2D mediated. (A) Levels of IFN-γ were measured after co-culture of NK:PCI-15B (1:1 ratio) or DC:NK:PCI-15B (1:1:1 ratio) with no treatment or with IgG1 or cetuximab (each at 10μg/ml) after 24h by ELISPOT assay. Furthermore, the molecular mechanism that may modulate NK-DC cross-talk was assessed by using anti-NKG2D Ab or anti-IL-12 Ab or anti-NKp30 Ab or anti-IL-18 Ab along with cetuximab (each at 10μg/ml) in parallel assays. A two-tailed unpaired t-test was performed for statistical analysis. Cumulative data of two donors are shown. (B) Enhancement by cetuximab of NK-DC cross-talk is dependent on MICA upregulation by DC. The level of NKG2D ligand MICA, on CD11c+ DC in co-cultures of NK:PCI-15B (1:1 ratio) or DC:NK:PCI-15B (1:1:1 ratio) with no treatment or with IgG1 or cetuximab (each at 10μg/ml, 48h) was measured by flow cytometry. A representative histogram is also shown.