Figure 4
Figure 4. Effect of neutralizing HCMV-induced IL-12 and IFNAR on NKG2D expression and NK-cell activation. PBMCs were incubated alone or with TB40/E in the presence or absence of antagonizing antibodies for IL-12, IL-15, and IFNAR. NKG2D (A) and CD69 (B) expression on CD56+CD3− cells was monitored at 72 hours by flow cytometry. (C) IFNγ secretion measured by ELISA in supernatants from cultures described in Figure 5A (mean ± SD). Results are representative of data obtained in at least 3 different donors. (D) PBMCs were incubated alone or with TB40/E in the presence or absence of antagonizing antibodies for IFNγ and IFNAR. NKG2D expression on CD56+CD3− cells was monitored at 72 hours by flow cytometry. Representative data of 1 of 2 donors tested are shown. Geometric mean values of mean fluorescence intensity are indicated in all histograms.

Effect of neutralizing HCMV-induced IL-12 and IFNAR on NKG2D expression and NK-cell activation. PBMCs were incubated alone or with TB40/E in the presence or absence of antagonizing antibodies for IL-12, IL-15, and IFNAR. NKG2D (A) and CD69 (B) expression on CD56+CD3 cells was monitored at 72 hours by flow cytometry. (C) IFNγ secretion measured by ELISA in supernatants from cultures described in Figure 5A (mean ± SD). Results are representative of data obtained in at least 3 different donors. (D) PBMCs were incubated alone or with TB40/E in the presence or absence of antagonizing antibodies for IFNγ and IFNAR. NKG2D expression on CD56+CD3 cells was monitored at 72 hours by flow cytometry. Representative data of 1 of 2 donors tested are shown. Geometric mean values of mean fluorescence intensity are indicated in all histograms.

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