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. Author manuscript; available in PMC: 2011 Aug 19.
Published in final edited form as: Cell Host Microbe. 2010 Aug 19;8(2):174–185. doi: 10.1016/j.chom.2010.07.008

Figure 4.

Figure 4

Resistance to poxvirus infection correlates with early and potent STAT network activation in dendritic cells and T cells.

(A) Ectromelia virus infection produces delayed and reduced pSTAT1 and pSTAT3 induction, especially in sensitive BALB/c mice. In vivo time course of the early immune responses in C57BL/6 and BALB/c mice infected intravenously with 1 × 107 pfu of either vaccinia virus or ectromelia virus (Moscow strain) was determined as in Figure 1. Percentage of cells demonstrating pSTAT1 or pSTAT3 activation at different times after infection is plotted for conventional dendritic cells (CD11c+), T cells (CD4+ or CD8+), B cells (B220+), and granulocytes (CD11bhi) (data represented as mean ± SD).

(B) Ectromelia virus induction of pSTAT3 is IL-6- but not TLR2-dependent. Wild-type (C57BL/6), TLR2−/−, and IL6−/− mice were infected with 1 × 107 pfu ectromelia virus. After 1 hour spleens were excised, dissociated, and prepared for intracellular analysis. Levels of pSTAT3 in CD11c+ cells are shown (data represented as mean +/− SD; two-tailed, unpaired t-test: * p<0.02 for IL6−/− compared to WT and TLR2−/−, WT compared to TLR2−/− was not significant).

(C) IL-6 induction is necessary for resistance to ectromelia virus infection in C57BL/6 mice. Wild-type and IL6−/− mice of the C57BL/6 background were subcutaneously infected with 1 × 103 pfu of ectromelia virus. Survival was monitored for 20 days following infection. Livers were extracted from separate groups of infected mice on day 7 and a plaque-forming assay was used to monitor viral burden.

(D) TLR2 activation prior to ectromelia infection reduces viral burden. PBS, 1 × 107 pfu of MVA (modified vaccinia Ankara), or 20 μg of PAM3CSK4 was intravenously injected into C57BL/6 mice one hour before systemic infection with 1 × 107 pfu of ectromelia. Spleens were excised 72 hours later and ectromelia burden was quantified using a plaque-forming assay (data represented as mean ± SD; two-tailed, unpaired t-test: * p< 0.01 MVA compared to PBS, p< 0.007 PAM3CSK4 compared to PBS).