Figure 8. PTX3 deficiency mitigates IgG responses to particulate but not soluble TD antigens. (A) ELISA of serum NP-specific IgG2b and IgG2c from WT and Ptx3−/− mice at day 14 after i.p. immunization with NP-OVA and alum. RU, relative units. (B) IFA of spleens stained for MMP9 (green) and B220 (red) from WT mice i.n. infected with PR8 influenza virus. Ctrl, control. Bars, 50 µm. (C and D) Flow cytometric analysis of absolute numbers of NBh cells (C) and MZ B cells (D) from WT and Ptx3−/− mice i.n. infected with PR8 influenza virus. (E) Serum PR8-specific IgG2c in WT and Ptx3−/− mice i.n. infected with PR8 influenza virus. Data summarize one to two experiments with at least three mice in each experimental group (A and C–E) or show one representative experiment of three with similar results (A). Error bars, SEM. *, P < 0.05 (two-tailed Student’s t test).
Figure 8.

PTX3 deficiency mitigates IgG responses to particulate but not soluble TD antigens. (A) ELISA of serum NP-specific IgG2b and IgG2c from WT and Ptx3−/− mice at day 14 after i.p. immunization with NP-OVA and alum. RU, relative units. (B) IFA of spleens stained for MMP9 (green) and B220 (red) from WT mice i.n. infected with PR8 influenza virus. Ctrl, control. Bars, 50 µm. (C and D) Flow cytometric analysis of absolute numbers of NBh cells (C) and MZ B cells (D) from WT and Ptx3−/− mice i.n. infected with PR8 influenza virus. (E) Serum PR8-specific IgG2c in WT and Ptx3−/− mice i.n. infected with PR8 influenza virus. Data summarize one to two experiments with at least three mice in each experimental group (A and C–E) or show one representative experiment of three with similar results (A). Error bars, SEM. *, P < 0.05 (two-tailed Student’s t test).

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