IL-4 and IL-13 activate the JAK2 tyrosine kinase and Stat6 in cultured human vascular endothelial cells through a common pathway that does not involve the gamma(c) chain
IL-4 and IL-13 activate the JAK2 tyrosine kinase and Stat6 in cultured human vascular endothelial cells through a common pathway that does not involve the gamma(c) chain
复制标题
DOI：
10.1172/jci118829
复制
发表时间：
1996-08-01
影响因子：
15.9
通讯作者：
Pober, JS
中科院分区：
文献类型：
--
作者：
PalmerCrocker, RL;Hughes, CCW;Pober, JS
IL-4和IL-13各自作用于人内皮细胞（EC）以诱导血管细胞粘附分子-1的表达。在造血细胞上，IL-4应答可以通过涉及g（c）（IL-2、IL-4、IL-7、IL-9和IL-15受体的共同信号传导亚基）的途径介导，或者通过可以被IL-13替代地激活的g（c）非依赖性途径介导。我们发现，人内皮细胞不表达g（c），通过间接免疫荧光和FACS（R）分析或通过逆转录PCR方法检测。像IL-4一样，IL-13激活使IL-4 R结合蛋白磷酸化的蛋白酪氨酸激酶。此外，我们发现IL-4和IL-13均诱导JAK 2酪氨酸激酶的酪氨酸磷酸化。此外，IL-4和IL-13均诱导Stat 6转录因子与共有序列寡核苷酸的结合。我们得出结论，人EC的IL-4应答涉及IL-13共享途径，该途径不依赖于g（c），并且使用JAK 2-Stat 6信号传导。
IL-4 and IL-13 each act on human endothelial cells (ECs) to induce expression of vascular cell adhesion molecule-1. On hematopoietic cells, IL-4 responses may be mediated either through a pathway involving g(c), the common signaling subunit of the IL-2, IL-4, IL-7, IL-9, and IL-15 receptors, or through a g(c)-independent pathway that may be alternatively activated by IL-13. We find that human ECs do not express g(c), as detected by indirect immunofluorescence and FACS(R) analysis or by a reverse transcription-PCR method. Like IL-4, IL-13 activates a protein tyrosine kinase that phosphorylates the IL-4R binding protein. In addition, we find that IL-4 and IL-13 each induce tyrosine phosphorylation of the JAK2 tyrosine kinase, Furthermore, both IL-4 and IL-13 induce binding of the Stat6 transcription factor to a consensus sequence oligonucleotide, We conclude that the IL-4 response of human ECs involves the IL-13 shared pathway that is independent of g(c), and uses JAK2-Stat6 signaling.