Fig 1: Infection triggers type I IFN–independent reductions in myeloid cell surface IFNGR1 that are dependent on type II IFN (IFN?).WT C57BL/6 mice were injected i.p. with 0.5 mg of a-IFN?, a-IFNAR1, both antibodies, or PBS vehicle control 24 h before i.v. infection with 104 CFU L. monocytogenes. (A, B) At 0, 24, or 72 hpi, splenocytes were harvested for FACS analysis. Splenic monocytes were gated as detailed in the Materials and Methods section. Relative changes in gMFI for IFNGR1 staining is shown versus control staining for three pooled experiments at each time point. (C) Serum IFN? concentrations at the indicated times after infection. Data are pooled from three experiments with a total of 7–9 mice/group. (D, E, F) Relative normalized transcript abundance of Ifng, Ifnb, or Ifna subtypes from lysed whole splenocytes at indicated times after infection. Data are pooled from three experiments with a total of 4–9 mice/group. (A, B, C, D, E, F) For all panels, error bars represent SEM; ***P < 0.001 as determined by one-way ANOVA and Dunnett’s (A, B) or Tukey’s (C, D, E, F) post-hoc tests for comparison between uninfected and other groups or comparison between conditions. n.s., not significant.
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