FIG 2.

IRF5 enhances influenza A virus-induced inflammatory response in a murine infection model. (A) Weight loss of WT and Irf5^−/− mice was assessed over time, and comparable results were observed in 4 independent experiments, with 4 to 5 WT or Irf5^−/− mice in each group per experiment. Data shown are the mean ± SEM. (B) Replication of virus in the lungs was quantified using a plaque assay. Data shown are the mean ± SEM using 7 WT and 5 Irf5^−/− mice for day 2 and 5 mice of each genotype for day 4. (C) Recruitment of specific myeloid cell populations (mDCs, monocyte-derived DCs; cDCs, conventional DCs; pDCs, plasmacytoid DCs; Inflam. mon, inflammatory monocytes) in WT and Irf5^−/− mice was assessed by flow cytometry 2 days p.i. Populations were defined by the following markers: alveolar macrophages (Alveolar macs), SiglecF⁺ CD11b⁺ CD64⁺ Ly6C⁻; mDCs, SiglecF⁻ CD11b⁺ MHC-II⁺ CD11c⁺ CD64⁺ Ly6C⁺; interstitial macrophages, SiglecF⁻ CD11b⁺ MHC-II⁺ CD11c⁻ CD64⁺ Ly6C⁺; inflammatory monocytes, SiglecF⁻ CD11b⁺ MHC-II⁻ Ly6C⁺ CD64⁺; cDCs, MHC-II⁺ CD11c⁺ Ly6C⁻; pDCs, B220⁺ SiglecH⁺ MHC-II^low CD11c^low; and eosinophils, SiglecF⁺ CD11c⁻ CD11b⁺ Ly6C⁻. Data shown are the mean ± SEM using 11 WT and 10 Irf5^−/− mice from multiple replicates. (D) The total number of each individual myeloid cell population (unstimulated, ex vivo) positive for IL-6 and TNF-α expression was detected by flow cytometry, with data presented representing the mean total cell number per 10⁵ cells of each cell type ± SEM. Data represent two experiments.