Figure 4
Figure 4. Intracellular IFN-γ staining of PBMCs incubated with allogeneic latently infected myeloid progenitor cells. Mock-, AD169-, and RVAdIL10C-infected myeloid progenitors harvested at days 3, 5, and 8 after infection were mixed (1:10) with PBMCs for 16 hours and assayed for intracellular IFN-γ using flow cytometry. The mitogen PHA was added to PBMCs as a positive control (PBMC + PHA), with PBMCs alone as a negative control. (A) Representative flow cytometry scatter plots of IFN-γ+ live-gated PBMCs for different treatments. (B) Column graphs showing mean fold change in the percentage of IFN-γ+ PBMCs after coculture with AD169- or RVAdIL10C-infected myeloid progenitors, normalized to mock-infected myeloid progenitor cells. The number of independent replicates (n) is shown. Significant differences between AD169 and RVAdIL10C treatments were determined using 1-tailed, paired Student t test: *P < .05, **P < .005.

Intracellular IFN-γ staining of PBMCs incubated with allogeneic latently infected myeloid progenitor cells. Mock-, AD169-, and RVAdIL10C-infected myeloid progenitors harvested at days 3, 5, and 8 after infection were mixed (1:10) with PBMCs for 16 hours and assayed for intracellular IFN-γ using flow cytometry. The mitogen PHA was added to PBMCs as a positive control (PBMC + PHA), with PBMCs alone as a negative control. (A) Representative flow cytometry scatter plots of IFN-γ+ live-gated PBMCs for different treatments. (B) Column graphs showing mean fold change in the percentage of IFN-γ+ PBMCs after coculture with AD169- or RVAdIL10C-infected myeloid progenitors, normalized to mock-infected myeloid progenitor cells. The number of independent replicates (n) is shown. Significant differences between AD169 and RVAdIL10C treatments were determined using 1-tailed, paired Student t test: *P < .05, **P < .005.

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