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. 2007 Jan 29;75(4):1690–1697. doi: 10.1128/IAI.01564-06

FIG. 2.

FIG. 2.

Functional characterization of IL-22BP-Fc. (A) Treatment of Hepa1-6 cells with rIL-22, but not rIL-10 or rFc, leads to STAT3 activation. Hepa1-6 cells were treated with 50 ng/ml rIL-22 or rIL-10 for 30 min. Lysates of Hepa1-6 cells were analyzed by Western blotting against STAT3 and phosphorylated STAT3. (B and C) rIL-22BP-Fc, but not rFc, inhibits rIL-22-induced STAT3 phosphorylation in Hepa1-6 cells. Fifty nanograms of rIL-22 per milliliter was incubated with indicated concentrations of rIL-22BP-Fc or rFc (0 to 2 μg/ml) for 10 min. Then, the mixtures were incubated for 30 min with Hepa1-6 cells. Cell lysates were analyzed by Western blotting with antibodies to STAT3 and phosphorylated STAT3. Western blots representative of three independent experiments are shown. (D) After densitometry, the concentration of IL-22BP-Fc yielding 50% inhibition of IL-22-induced STAT3 phosphorylation was calculated to be 0.25 μg/ml. (E) BMDC were treated with 50 ng/ml rIL-22 or rIL-10 for 30 min in the presence of rIL-22BP-Fc (10 μg/ml). Lysates were analyzed by Western blotting against STAT3 and phosphorylated STAT3.