Fig. 1.

Survival of TLR11-deficient mice during acute toxoplasmosis depends on IFN-γ but not NK or T cells. TLR11^−/− mice were infected intraperitoneally (i.p.) with 20 cysts of the ME49 strain of T. gondii and were additionally treated with IFN-γ blocking antibody (red), αNK1.1, αCD4 and αCD8 antibodies to simultaneously deplete NK and T cells (green), or vehicle control (blue) (A). The survival of the TLR11^−/− mice was compared with similarly infected IFN-γ^−/− mice (black). P ≤ 0.009. (B) Infected TLR11^−/− mice were treated with IFN-γ–blocking antibody (red), or αNK1.1, αCD4, or αCD8 antibodies to individually deplete NK and CD4 or CD8 T cells, respectively, or vehicle control (blue). T. gondii load and IFN-γ production in the peritoneal cavity of infected mice were analyzed 5 d after infection by quantitative RT-PCR and ELISA, respectively. (C) T. gondii load and IFN-γ production in the peritoneal cavity of infected mice were analyzed on day 5 after infection by quantitative RT-PCR and ELISA, respectively. The data shown are one of three experiments, each involving five mice per group, “ns” is not significant, and error bars shown are the means ± SEM.