PROLACTIN AND INTERLEUKIN-2 RECEPTORS IN T-LYMPHOCYTES SIGNAL THROUGH A MGF-STAT5-LIKE TRANSCRIPTION FACTOR
PROLACTIN AND INTERLEUKIN-2 RECEPTORS IN T-LYMPHOCYTES SIGNAL THROUGH A MGF-STAT5-LIKE TRANSCRIPTION FACTOR
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DOI：
10.1210/en.136.12.5700
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发表时间：
1995-12-01
期刊：
影响因子：
4.8
通讯作者：
GRONER, B
中科院分区：
文献类型：
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作者：
GOUILLEUX, F;MORITZ, D;GRONER, B
PRL和白细胞介素-2（IL-2）的细胞表面受体在结构上不同，但在T淋巴细胞中共享调节任务。它们可以刺激增殖并激活T细胞的重叠基因组的转录。PRL和IL-2受体激活均与Jak/Stat（信号转导和转录激活因子）途径相关。我们研究了PRL和IL-2激活不同T细胞系中Stat蛋白的能力。研究了Nb 2和Cl 96 T细胞系中的DNA结合特异性、对STAT特异性抗血清的反应性以及IL-2和PRL诱导的DNA结合蛋白的分子量。与干扰素-γ、PRL和IL-6在T47 D乳腺肿瘤细胞中诱导的Stat蛋白进行比较。我们发现，这些参数是不可区分的PRL和IL-2诱导的因素之一。与乳腺因子密切相关的转录因子Stat 5在IL-2和PRL与其各自的受体相互作用时被迅速激活。还观察到与Stat 1相关的第二种蛋白质的激活。我们的研究结果强调了PRL作为免疫应答调节剂的作用，并表明Stat因子乳腺因子-Stat 5和Stat 1在T细胞发育过程中的基因表达调节中发挥作用。
The cell surface receptors for PRL and interleukin-2 (IL-2) are structurally distinct, but share regulatory tasks in T lymphocytes. They can stimulate proliferation and activate transcription of overlapping sets of genes of T cells. PRL and IL-2 receptor activation are both linked to the Jak/Stat (signal transducer and activator of transcription) pathway. We investigated the ability of PRL and IL-2 to activate Stat proteins in different T cell lines. The DNA binding specificities, the reactivities toward Stat-specific antisera, and the mol wt of IL-2- and PRL-induced DNA-binding proteins in Nb2 and Cl96 T cell lines were investigated. A comparison with the Stat proteins induced by interferon-gamma, PRL, and IL-6 in T47D mammary tumor cells was made. We found that these parameters were indistinguishable for one of the PRL- and IL-2-induced factors. A transcription factor closely related to mammary gland factor-Stat5 is rapidly activated upon interaction of IL-2 and PRL with their respective receptors. Activation of a second protein related to Stat1 was also observed. Our results emphasize the role of PRL as a regulator of the immune response and indicate that the Stat factors mammary gland factor-Stat5 and Stat1 play a role in the regulation of gene expression during T cell development.