Figure 3
Figure 3. CFSE proliferation assay of PBMC incubated with allogeneic latently infected myeloid progenitor cells. CFSE-labeled PBMCs were incubated for 5 days with mock-, AD169-, and RVAdIL10C-infected myeloid progenitors (harvested at days 3, 5, 8, 11, and 14 after infection) and assayed for proliferation using flow cytometry. The mitogen phytohemagglutinin (PHA) was added to PBMC as a positive control (PBMC + PHA), with CFSE-labeled PBMCs (PBMC only) as negative control. (A) Representative histogram plots of live-gated PBMCs undergoing proliferation measured by CFSE are shown. (B) Mean fold change in the percentage of PBMC proliferation in response to AD169- or RVAdIL10C-infected myeloid progenitors normalized to mock-infected myeloid progenitor cells. The number of independent replicates performed for each time point is indicated by n. Significant differences between AD169 and RVAdIL10C treatments were determined using 1-tailed, paired Student t test: *P < .05, ***P < .001.

CFSE proliferation assay of PBMC incubated with allogeneic latently infected myeloid progenitor cells. CFSE-labeled PBMCs were incubated for 5 days with mock-, AD169-, and RVAdIL10C-infected myeloid progenitors (harvested at days 3, 5, 8, 11, and 14 after infection) and assayed for proliferation using flow cytometry. The mitogen phytohemagglutinin (PHA) was added to PBMC as a positive control (PBMC + PHA), with CFSE-labeled PBMCs (PBMC only) as negative control. (A) Representative histogram plots of live-gated PBMCs undergoing proliferation measured by CFSE are shown. (B) Mean fold change in the percentage of PBMC proliferation in response to AD169- or RVAdIL10C-infected myeloid progenitors normalized to mock-infected myeloid progenitor cells. The number of independent replicates performed for each time point is indicated by n. Significant differences between AD169 and RVAdIL10C treatments were determined using 1-tailed, paired Student t test: *P < .05, ***P < .001.

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