IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis
J. Clin. Invest. Ken Sugimoto, et al. 118:534 doi:10.1172/JCI33194 [Go to this article.]

Figure 1
Enhancement of STAT3 activation in CECs by IL-22. (A) Expression levels of IL-22 in normal colon of WT (n = 9) and inflamed colon of TCRαKO (TCRα) mice (n = 9) and the CD45RB colitis model (n = 4). (B) Expression levels of IL-22 in intestinal biopsy samples from healthy controls (n = 10) and from patients with UC (n = 12) or CD (n = 9) are shown. (C) Expression levels of IL-22 in purified CD4⁺ T cells and IgM⁺ cells from inflamed colon of TCRαKO mice are shown. (D) Expression levels of IL-22 in purified CD4⁺ T cells from inflamed colon of TCRαKO mice and CD45RB model are shown. (E) Expressions of β-actin, IL-22RA1, and IL-10R2 in CECs (red lines) and colonic LP (black lines) of TCRαKO mice. Results represent averages of 4 different experiments ± SEM. Quantitative data relative to β-actin expression are summarized in the 2 right panels. (F and G) Freshly isolated CECs from WT mice were stimulated with various doses of IL-22 for 15 minutes (F). Normal human colonic tissues were stimulated without (cont) or with 10 ng/ml of IL-22 (G). Protein lysates (10 μg) were immunoblotted with anti–phospho-STAT3 (P-STAT3) or anti–phospho–ERK1/2 Abs. After stripping the Abs, the membrane was reprobed with anti-STAT3 or anti-ERK1/2 Abs. The result is representative of 3 individual experiments. (H) Human colonic specimen was stimulated without (top panel) or with IL-22 (bottom panel) for 2 hours and subjected to immunohistochemical analysis using anti–phospho-STAT3 Abs. Original magnification, ×40.