Contribution of STAT1 to regulation of CD8 T-cell proliferation. (A) CD8 T cells from wild-type or STAT1-deficient mice proliferate in response to growth factors in culture, but STAT1 is required for the antiproliferative effects mediated by type 1 IFN. Total splenic populations were prepared from uninfected mice, CFSE-labeled on day 0, and cultured for 5 days in the absence or presence of IFNα (1 × 10⁴ U/mL), with or without IL-2, IL-7, or IL-15 (20 ng/mL each). Flow cytometry histogram plots of gated CD8 T cells are shown. Numbers are proportions of cells dividing as assessed by dilution of CFSE. (B) STAT1 contributes to the negative regulation of early CD8 T-cell proliferation in vivo during LCMV infection. Wild-type and STAT1-deficient mice were infected with LCMV and followed for 4 days after infection, and CD8 T-cell proliferation was measured by BrdU incorporation in vivo. Proportions and numbers of total, as well as BrdU-positive CD8 T cells, are shown. Active IFNα/β in serum was measured by bioassay and serum IFNα by ELISA. All data are means ± SDs. Results for both panels are representative of at least 3 independent experiments.