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. 2014 Jun;34(12):2235–2248. doi: 10.1128/MCB.00295-14

FIG 7.

FIG 7

STAT1α and STAT1β show differential efficiencies in immune defense against MCMV and L. monocytogenes infections. (A) WT (Stat1+/+), Stat1β/β, Stat1α/α, and Stat1−/− mice were infected i.p. with MCMV (4 × 105 PFU/mouse), and survival was monitored for 14 days. The data are derived from two independent experiments; n = 20 (Stat1+/+), n = 23 (Stat1β/β), n = 14 (Stat1α/α), and n = 18 (Stat1−/−). Significances were as follows: Stat1β/β versus all others, P < 0.01; Stat1−/− versus WT and Stat1α/α, P < 0.001. (B) WT (Stat1+/+), Stat1β/β, Stat1α/α, and Stat1−/− mice were infected i.p. with L. monocytogenes (2 × 105 CFU/mouse), and survival was monitored for 14 days. The data are derived from four independent experiments. n = 39 (Stat1+/+), n = 34 (Stat1β/β), n = 21 (Stat1α/α), and n = 17 (Stat1−/−). Significances were as follows: Stat1β/β versus all others, P < 0.0001; Stat1−/− versus all others, P < 0.0001. (C) Mice were infected as for panel B and killed 3 or 5 days postinfection. Whole spleens and livers were removed and homogenized, and bacterial loads were determined with standard CFU assays. The data are from two independent experiments. Days 3 and 5, n = 11 and 9 (Stat1+/+), n = 11 and 12 (Stat1β/β), n = 13 and 11 (Stat1α/α), and n = 8 and 0 (Stat1−/−); because of their early lethality after infection, Stat1−/− mice had to be excluded from the analysis at day 5. **, P ≤ 0.01; ***, P ≤ 0.001.