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. 2016 Mar 22;6:23475. doi: 10.1038/srep23475

Figure 2. Impaired production of IFN-γ in the adipose tissue of infected IL-12/IL-23 p40−/− mice.

Figure 2

Frequencies of (a) IFN-γ+ NK1.1+ TCRβTCRγδ cells on total NK1.1+ cells, (b) IFN-γ+ NK1.1+ TCRβ+ TCRγδ cells on total NK1.1+ TCRβ+ cells, (c) IFN-γ+ TCRγδ+ NK1.1 cells on total TCRγδ+ cells, (d) IFN-γ+ IL-10CD8+ TCRβ+ TCRγδNK1.1 cells on total CD8+ T cells and (e) IFN-γ+ IL-10CD4+ TCRβ+ TCRγδNK1.1, IFN-γ+ IL-10+ CD4+ TCRβ+ TCRγδNK1.1 and IL-10+ IFN-γCD4+ TCRβ+ TCRγδNK1.1 cells on total CD4+ T cells in the mesenteric and subcutaneous adipose tissue (MAT and SAT, respectively) from IL-12/IL-23 p40−/− mice sacrificed 24 h after intraperitoneal challenge with 1 × 107 N. caninum tachyzoites (NcT) or PBS, as indicated. Each symbol represents an individual mouse. Bars represent means of 7–9 mice per group pooled from 2 independent experiments. (Mann-Whitney U, **P ≤ 0.01). Representative example of gating strategy used to define the respective cellular populations in the different depots of adipose tissue analysed. The example shown corresponds to MAT.