Skip to main content
. Author manuscript; available in PMC: 2010 Jul 12.
Published in final edited form as: Nat Med. 2008 Feb 10;14(3):275–281. doi: 10.1038/nm1710

Figure 1.

Figure 1

Primary HBE cells express IL-22R, and stimulation with IL-22 and IL-17A leads to the upregulation of host defense genes and increases clonogenic frequency. (a) Primary HBE cells were stained with a goat antibody to IL-22R. Fifteen percent of HBE cells were positive for IL-22R (red); controls with secondary antibody only are shown in purple. (b) Heat map of genes expressed in HBE cells after 24 h stimulation with media, 20 ng/ml IL-22, 10 ng/ml IL-17A or a combination of 20 ng/ml IL-22 and 10 ng/ml of IL-17A (n = 3 per condition). (c) G-CSF abundance in basolateral media of HBE cells after stimulation with IL-17A, IL-22 or both (n = 5–6 from three individual donors per condition). (d) IL6 abundance in basolateral media of HBE cells after stimulation with IL-17A, IL-22 or both (n = 5–6 from three individual donors per condition). (e) Primary HBE cells were seeded at specific densities into a 96-well plate containing media, 200 ng/ml of IL-22 or 100 ng/ml of IL-17A. IL-22 increased the clonogenicity of cells more than IL-17A or media alone did (n = 3–4 from three individual donors per condition). (f) We developed 10-μm wounds in primary HBE cells before stimulating them with media alone or 20 ng/ml of IL-22 (n = 5–6 from three individual donors per condition). For c–f, *P < 0.05 compared with media control and error bars represent means ± s.e.m.