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. 2013 Jun 10;110(26):10711–10716. doi: 10.1073/pnas.1307868110

Fig. 2.

Fig. 2.

IFN-γ production by non-NK non-T cells in T. gondii-infected mice. (A) WT and TLR11−/− mice were infected i.p. with T. gondii and IFN-γ+ cells were identified in the peritoneal cavity of infected mice by gating on live IFN-γ+ cells on day 5 after infection. IFN-γ+ cells were further differentiated by plotting NK1.1 vs. CD3ε as markers for NK and T cells, respectively. (B) Relative (Upper) and absolute quantification (Lower) of total IFN-γ+ cells (Left) and additionally broken down by cell types (Right) in WT (white) and TLR11−/− (black) mice. (C) IFN-γ+ cells were identified in the peritoneal cavity of infected RAG/IL-2Rγc−/− mice by gating on live IFN-γ+ cells (Upper) and total IFN-γ expression in infected WT, TLR11−/−, and RAG/IL-2Rγc−/− was measured on day 5 after infection by RT-PCR (Lower). P ≤ 0.04. (D) Cell surface markers expressed by IFN-γ+ CD3ε NK1.1 cells isolated from T. gondii-infected TLR11−/− mice (open histograms) compared with appropriate isotype controls (filled histograms). The data shown are one of four experiments each involving 3–5 mice per group. Error bars are means ± SEM.