Figure 2.

T-cell and NK-cell activation during M. bovis BCG infection were not deficient in IFN-αβR^–/– lungs. Mice were infected by aerosol with 3000–4500 BCG and lung cells were prepared for flow cytometry. (a–d) Lung T cells from wild-type (a, b) and IFN-αβR^–/– mice (c,d) were stained for CD3, CD4, CD69 and CD25. CD3⁺/CD4⁺ T cells, shown within the gates of scatter plots from individual mice (a,c), were analysed for expression of CD69 (b,d) and CD25 (not shown). Histograms using data from three wild-type or IFN-αβR^–/– mice are shown from day 22 post-infection (b,d), when T-cell numbers were maximal. Each open histogram represents a single mouse, and shaded histograms are isotype controls. The mean (± SD) total number of cells/lung (× 10⁻⁶) is indicated for CD4⁺ T cells (a,c) and CD4⁺ CD69⁺ T cells (b,d) and were not significantly different between wild-type and IFN-αβR^–/– mice. Similar results were observed for two separate high-dose infection experiments. (e–h) Lung NK cells from wild-type (e,f) and IFN-αβR^–/– mice (g,h) were stained for CD3, DX5 and CD69. CD3^– DX5⁺ NK cells, shown within the gates of representative scatter plots from individual mice (e,g), were analysed for expression of CD69 (f,h). Histograms from an experiment with three wild-type and IFN-αβR^–/– mice are shown for day 21 post-infection. Each open histogram represents a single mouse, and shaded histograms are isotype controls. The mean (± SD) total number of cells/lung (× 10⁻⁶) is indicated for NK cells (CD3^– DX5⁺, e,g) and CD69⁺ NK cells (f,h) and were not significantly different between wild-type and IFN-αβR^–/– mice. Similar results were observed for two separate high-dose infection experiments.