Ruxolitinib therapy improves the survival of infected Prf1^−/− mice and suppresses STAT1 activation in vivo. (A) Control (B6) and perforin-deficient (Prf1^−/−) mice infected with LCMV on day 0 were treated with either JAK1/2 inhibitor (ruxolitinib) or vehicle solution alone from day 7 to day 28 (21 days treatment; left) or from day 7 to day 21 (14 days treatment; right). A group of Prf1^−/− mice was treated with anti-IFNγ antibody given every third day from day 7 until day 16. Data (mean ± SEM) are representative of 3 to 4 independent experiments with at least 3 mice in each group. **P < .005; ****P < .0001. Survival was analyzed with a log-rank test (Mantel-Cox) (n = 5-17). (B, left) Representative fluorescence-activated cell sorter analysis of pStat1 levels in the blood MNCs from control (B6) and Prf1^−/− mice treated with ruxolitinib or not and analyzed at 2 different times. (Right) Quantification of mean fluorescence intensity of pStat1 in the blood MNCs from control and Prf1^−/− mice treated with ruxolitinib or not at the day postinfection indicated. At each point, measurement was performed 1 hour after gavage with ruxolitinib. ND, not determined for nontreated Prf1^−/− mice that do not survive. Data (mean ± SD) represent 3 to 4 mice in each group. ***P < .001; ****P < .0001.