Fig. 5.

CD8⁺ T cells and endogenous IFN-γ are necessary for monocyte derived dendritic cells differentiation and activation as well as lung damage. a MA-ARDS/ALI-induced hemorrhage is attenuated in the lungs of PbN-infected β2-microglobulin^−/− and IFN-γ^−/− mice, compared to WT mice. b Delayed mortality in PbN-infected WT, β2-microglobulin^−/−, and IFN-γ^−/− mice. c Expression of CXCL9 and CXCL10 mRNA in the lungs of uninfected and PbN-infected WT, β2-microglobulin^−/−, and IFN-γ^−/− mice. d Histogram illustrating the expression of DCsign (left panel) and CD11c (right panel) in F4/80⁺CD11b⁺Ly6c⁺ cells in the lungs from control (uninfected) and PbN-infected WT, β2-microglobulin^−/−, and IFN-γ^−/− mice. e MFI bar graphs relative to the histograms of DCsign and CD11c shown in (d). f ELISA quantification of IFN-γ and TNF-α levels in lung homogenates from control and PbN-infected WT mice. f Number of IFN-γ producing CD4⁺ T and CD8⁺ T cells from lungs of control and PbN-infected C57BL/6 mice. g Numbers of CD11b⁺Ly6c⁺ TNFα⁺NOS2⁺ cells (Tip-DCs) from WT and 2-microglobulin^−/− mice. Data (a–g) are representative of two independent experiments (n = 4–5 mice per group)