FIG 6.

IFN-γ induces pathogen-specific IgM production during IOE infection in the absence of Ifnar signaling. Plasmablasts (B220^lo CD11c^lo) and serum Ehrlichia-specific IgM were measured at different time points post-IOE infection as indicated. (A) Representative flow cytometric plots of plasmablasts in the spleens of WT and Ifnar^−/− mice at day 8 postinfection are shown. The numbers (means ± SD) above the circle gates represent the frequency of plasmablasts. (B) The absolute numbers of splenic plasmablasts are shown. (C) Titers of serum OMP-19-specific IgM in WT and Ifnar^−/− mice at days 9 and 10 postinfection are shown. (D) Representative flow cytometric plots of WT (CD45.1⁻ CD45.2⁺ GFP⁺) and Ifnar^−/− (CD45.1⁻ CD45.2⁺ GFP⁻) plasmablasts in spleens of mixed BM chimeric mice at day 7 postinfection are shown. The numbers in the quadrants represent the percentage of WT or Ifnar^−/− cells among total splenic plasmablasts. (E) Quantification of percentage of WT and Ifnar^−/− plasmablasts in panel D is shown. (F) Representative flow cytometric plots of splenic plasmablasts on day 8 postinfection in Ifnar^−/− mice with or without anti-IFN-γ treatment are shown. The numbers above the gate represent the percentage of plasmablasts among all splenocytes. (G) Quantification of plasmablasts in panel F is shown. (H) Titers of serum OMP-19-specific IgM in Ifnar^−/− mice with or without anti-IFN-γ treatment at day 8 postinfection are shown. Asterisks indicate a significant difference compared to uninfected controls (P < 0.05). Number symbols (#) indicate a significant difference between the groups as indicated (P < 0.05). “n.s.” indicates no significant difference (P > 0.05). “n.d.” indicates not detectable. At least four animals were used for each group.