Impact of viral IL-10 on CD4⁺ T-cell response to latently infected myeloid progenitor cells. (A-B) Allogeneic settings. (C-E) Autologous settings. Mock-, AD169-, and RVAdIL10C-infected myeloid progenitors harvested at day 8 after infection were mixed (1:10) with allogeneic CD4⁺ T cells and intracellular IFN-γ expression or cell proliferation determined by flow cytometry on CD3⁺/CD4⁺ cells from 4 independent replicate experiments (n). Column graphs show mean fold-change of the percentage of (A) IFN-γ⁺ CD3⁺/CD4⁺ T cells and (B) proliferative response of CFSE-labeled CD3⁺/CD4⁺ T cells to allogeneic AD169- and RVAdIL10C-infected myeloid progenitors. Significant differences between AD169 and RVAdIL10C treatments were determined using 1-tailed, paired Student t test. (C) Surface expression of MHC class II (HLA-DR) on mobilized peripheral blood-derived myeloid progenitor cells. Mock-, AD169-, and RVAdIL10C-infected CD34⁺ myeloid progenitors from 3 HCMV-seropositive and 3 HCMV-seronegative stem cell donors were harvested on day 8 after infection and assessed for surface MHC class II expression by flow cytometry. The mean fold change in the percentage of MHC class II–positive myeloid progenitors infected with AD169 or RVAdIL10C is shown relative to mock-infected counterparts. (D) Column graphs represent mean fold change (relative to mock infection) of the percentage of IFN-γ⁺ CD3⁺/CD4⁺ T cells and (E) proliferative response of CFSE-labeled CD3⁺/CD4⁺ T cells after incubation with autologous mock-, AD169-, and RVAdIL10C-infected myeloid progenitors from HCMV-seropositive and HCMV-seronegative stem cell donors. Significant differences between AD169 and RVAdIL10C infections using 3 HCMV-seropositive and 3 HCMV-seronegative donors were determined using 1-tailed, paired Student t test: *P < .05, **P < .005.