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. Author manuscript; available in PMC: 2008 Dec 1.
Published in final edited form as: Nat Med. 2008 May 18;14(6):633–640. doi: 10.1038/nm1770

Figure 4.

Figure 4

NKT cells drive IL-13R expression to upregulate IL-13 production and alternative activation of macrophages after viral infection. (a) Lung levels of Il-13ra1 mRNA in WT, Cd1d1−/−, and Il13−/− mice at Day 49 PI. (b) Levels of Il-13ra1 mRNA in macrophages (Mac1+ and CD3− NK1.1−GR1−B220−CD11c−) and non-macrophages (Mac1−) purified from WT and Cd1d1−/− mice at Day 49 PI. Similar results were obtained for Mac1+CD68+ versus Mac1+CD68− cell subsets (data not shown). For (a,b), (*) indicates a significant increase from SeV-UV. (c) Representative photomicrographs of lungs sections immunostained for CD68 and Il-13rα1 at Day 49 PI. Bar = 50 μm. (d) Quantitative analysis of IL-13+CD68+ macrophages in mice inoculated with SeV-UV or SeV and treated with either control IgG or sIL-13Rα2-Fc from Day 12 to 49 PI. (e) Lung levels of Il-13 mRNA determined for conditions in (d). For (d,e), (*) indicates significant decrease from control IgG. (f) Representative photomicrographs of lungs sections immunostained for CD68 and Chi3l3/4 at Day 49 PI. Bar = 50 μm. (g) Lung levels of Chi3l3/4 mRNA in WT, Il13−/−, and Cd1d1−/−mice at Days 21 and 49 PI. (h) Levels of Chi3l3/4, Arg1, and Mmp12 mRNA in lung macrophages purified from WT and Cd1d1−/− mice at Day 49 PI. For (g,h), (*) indicates a significant increase from corresponding SeV-UV value, and (**) indicates a significant decrease from corresponding WT control value.