Fig 4. Inhibition of type I interferon signaling removes the benefit of SOCS-1 inhibition.

A) Interferon levels in the skin at day 1 post-infection in SCR KIR and iKIR treated animals as measured via ELISA. B) Bacterial load as determined via CFU in skin biopsy homogenates of SCR KIR and iKIR treated mice treated with either IFNGR antibody or IgG control. C) Bioluminescent infection area in the skin of SCR KIR and iKIR treated animals treated with or without an IFNAR blocking antibody at day 1 post-infection. D) Bacterial load determined by CFU measured in the skin biopsy homogenates from mice treated as in C at day 1 post-infection. E) Representative images of bioluminescent MRSA in the skin of mice treated as in C using planar bioluminescent imaging with average flux (photons/sec) below F) Nitrite/Nitrate as measured via Griess assay from biopsies collected from mice treated as in C at day 1 post-infection. G) Surface lesion size as measured via caliper at day 3 post-infection in BALB/c or BALB/c IFNAR -/- mice treated with either iKIR or SCR KIR. H) Bacterial load determined by CFU measured in the skin biopsy homogenates from mice treated as in G at day 3 post-infection. I) Representative images of bioluminescent MRSA in the skin of mice treated as in G using planar bioluminescent imaging with average flux (photons/sec) below. J) Nitrite/Nitrate as measured via Griess assay from biopsies collected from mice treated as in I at day 3 post-infection. Data represent the mean ± SEM from 3–9 mice from 2–3 independent experiments. *p < 0.05 vs. SCR KIR+αIGG or SCR treated WT mice. #p<0.05 vs. iKIR+ αIGG or iKIR treated WT mice.