Lejeune Diane, Dumoutier Laure, Constantinescu Stefan, Kruijer Wiebe, Schuringa Jan Jacob, Renauld Jean-Christophe
Ludwig Institute for Cancer Research, Brussels Branch, Experimental Medicine Unit, Université de Louvain, avenue Hippocrate 74, B-1200 Brussels, Belgium.
J Biol Chem. 2002 Sep 13;277(37):33676-82. doi: 10.1074/jbc.M204204200. Epub 2002 Jun 26.
IL (interleukin)-22 is an IL-10-related cytokine; its main biological activity known thus far is the induction of acute phase reactants in liver and pancreas. IL-22 signals through a receptor that is composed of two chains from the class II cytokine receptor family: IL-22R (also called ZcytoR11/CRF2-9) and IL-10Rbeta (CRF2-4), which is also involved in IL-10 signaling. In this report, we analyzed the signal transduction pathways activated in response to IL-22 in a rat hepatoma cell line, H4IIE. We found that IL-22 induces activation of JAK1 and Tyk2 but not JAK2, as well as phosphorylation of STAT1, STAT3, and STAT5 on tyrosine residues, extending the similarities between IL-22 and IL-10. However our results unraveled some differences between IL-22 and IL-10 signaling. Using antibodies specific for the phosphorylated form of MEK1/2, ERK1/2, p90RSK, JNK, and p38 kinase, we showed that IL-22 activates the three major MAPK pathways. IL-22 also induced serine phosphorylation of STAT3 on Ser(727). This effect, which is not shared with IL-10, was only marginally affected by MEK1/2 inhibitors, indicating that other pathways might be involved. Finally, by overexpressing a STAT3 S727A mutant, we showed that serine phosphorylation is required to achieve maximum transactivation of a STAT responsive promoter upon IL-22 stimulation.
白细胞介素(IL)-22是一种与IL-10相关的细胞因子;迄今为止已知的其主要生物学活性是诱导肝脏和胰腺中的急性期反应物。IL-22通过一种受体发出信号,该受体由II类细胞因子受体家族的两条链组成:IL-22R(也称为ZcytoR11/CRF2-9)和IL-10Rβ(CRF2-4),后者也参与IL-10信号传导。在本报告中,我们分析了大鼠肝癌细胞系H4IIE中响应IL-22而激活的信号转导途径。我们发现IL-22诱导JAK1和Tyk2而非JAK2的激活,以及酪氨酸残基上STAT1、STAT3和STAT5的磷酸化,这扩展了IL-22与IL-10之间的相似性。然而,我们的结果揭示了IL-22和IL-10信号传导之间的一些差异。使用针对MEK1/2、ERK1/2、p90RSK、JNK和p38激酶磷酸化形式的特异性抗体,我们表明IL-22激活了三条主要的MAPK途径。IL-22还诱导了STAT3在Ser(727)处的丝氨酸磷酸化。这种IL-10所没有的效应仅受到MEK1/2抑制剂的轻微影响,表明可能涉及其他途径。最后,通过过表达STAT3 S727A突变体,我们表明丝氨酸磷酸化是在IL-22刺激下实现STAT反应性启动子最大反式激活所必需的。