FIG 8.

Transient IL-10R blockade early during E. muris infection enhances memory and secondary recall CD4⁺ T cell responses. (A) Schematic representation of anti-IL-10R antibody and antibiotic treatment and secondary challenge infection in E. muris-infected mice. E. muris-infected WT C57BL/6 mice were treated an IL-10R blocking MAb or an isotype control on days 0 and 5 postinfection. Both groups of mice were treated with a course of antibiotic for 7 days starting on day 10 after E. muris infection. Mice were challenged with a second dose of E. muris on day 70 after primary infection. CD4⁺ T cell responses were analyzed on day 65 after the primary infection and day 5 after the secondary infection. Tissue bacterial loads were determined after antibiotic treatment and day 5 after secondary challenge infection. (B to D) Percentage of antigen-specific CD49d^hi CD11a^hi cells within the CD4⁺ T cell population (B), production of IFN-γ after ex vivo antigenic stimulation (C), and mean fluorescence intensity (MFI) of IFN-γ (D) expressed by antigen-specific CD49d^hi CD11a^hi CD4⁺ T cells in the spleens of E. muris-infected WT mice treated with IL-10R blocking MAb or isotype control on day 65 postinfection. (E to G) Percentage of antigen-specific CD49d^hi CD11a^hi cells within the CD4⁺ T cell population (E), production of IFN-γ after ex vivo antigenic stimulation (F), and MFI of IFN-γ (G) expressed by antigen-specific CD49d^hi CD11a^hi CD4⁺ T cells in the spleens of E. muris-infected WT mice treated with IL-10R blocking MAb or isotype control on day 5 after secondary challenge infection. (H) Bacterial loads in the blood, liver, and lungs of E. muris-infected WT mice, treated with IL-10R blocking MAb or isotype control, on day 5 after secondary E. muris challenge. Bacterial loads were undetectable in the organs on days 20 and 65 postinfection after antibiotic treatment (data not shown). Data are representative of four or five mice per group and two independent experiments. *, P = 0.01 to 0.05; ***, P < 0.001.