Fig. 6

Several myeloid cell types upregulate FcγR4 expression upon P. berghei NK65 infection. C57BL/6 mice were infected with P. berghei NK65 and dissected at 8 dpi. Leukocytes were isolated from the lungs according to protocol 2 and flow cytometry was performed. The neutrophils (A; CD45⁺ Lin⁻ SiglecF⁻ CD11b⁺ Ly6G⁺), dendritic cells (B; CD45⁺ Lin⁻ SiglecF⁻ MHCII⁺ CD11c⁺), alveolar macrophages (C; CD45⁺ SiglecF⁺ CD11b^int CD11c⁺), interstitial macrophages (D; CD45⁺ Lin⁻ SiglecF⁻ Ly6G⁻ CD11b^hi MHCII⁺ CD24⁻ CD64⁺), Ly6C⁺ inflammatory monocytes (E; iMOs; CD45⁺ Lin⁻ SiglecF⁻ Ly6G⁻ CD11b^hi MHCII⁻ Ly6C⁺) and Ly6⁻ non-classical monocytes (F; ncMOs; CD45⁺ Lin⁻ SiglecF⁻ Ly6G⁻ CD11b^hi MHCII⁻ Ly6C⁻) in the lungs were gated and the intensity of FcγR4 was determined. Lineage gating was performed using CD3 and CD19. A–F Left graph: mean fluorescent intensity of FcγR4 was determined on each cell type. Each symbol represents data of an individual mouse. n = 6, for CON and d8. P-values were indicated as follows: *p < 0.05, **p < 0.01, ***p < 0.001. The horizontal black line in each group indicates the median. Right graph: representative histograms showing the normalized intensity of FcγR4 for the fluorescence minus one (FMO) control, an uninfected control mouse (CON) and a P. berghei NK65-infected mouse (d8)