Fig. 4.

Neutrophils produce IFN-γ in an IL-12–independent, TNF- and IL-1β–dependent manner. Mice were infected i.p. with 20 cysts of the ME49 strain T. gondii. (A) PEC were analyzed by flow cytometry on days 2, 3, 5, and 7. Total IFN-γ⁺ cells were examined by absolute quantification in WT (white) and TLR11^−/− mice (black). IL-12 in PEC CD11c⁺ DCs was examined by relative quantification of IL-12p40 expression from IL-12–reporter mice (Yet40) (white) and Yet40xTLR11^−/− mice (black). (B) Absolute quantification of IFN-γ⁺ Ly-6G⁺ cells day 5 after infection from TLR11^−/− mice that received control (black) or αIL-12 antibody (checkered). (C) T. gondii load in the peritoneal cavity of infected TLR11^−/− mice that received control (black), αIL-12 antibody (checkered), or αIFN-γ (gray) were analyzed on day 5 after infection by quantitative RT-PCR. P ≤ 0.004. (D) Absolute quantification of IFN-γ⁺ Ly-6G⁺ cells from infected TLR11^−/− mice that received control (white) or IL-1R antagonist (light gray) or αTNF antibody (hatched). P ≤ 0.05. (E) WT (white), TLR11^−/− (black), and IL-1R^−/− mice (light gray) were infected and then analyzed by absolute quantification of IFN-γ⁺ Ly-6G⁺ cells day 5 after infection. *P ≤ 0.05 and **P ≤ 0.002. The data shown are one of three independent experiments with three to seven mice per group, and error bars shown are the means ± SEM.