在真菌衍生的肿瘤T细胞中,白介素-2/白介素-15刺激下Gab2在酪氨酸上磷酸化,并诱导与SHP-2和Stat5a相关

J. Brockdorff, Haihua Gu, T. Mustelin, K. Kaltoft, C. Geisler, C. Röpke, N. Ødum
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引用次数: 15

摘要

皮肤T细胞淋巴瘤(CTCLs)常表现出异常的白细胞介素-2 (IL-2)受体信号。在这项研究中,我们研究了Gab2的作用,这是一种最近发现的与IL-2受体信号传导有关的接头分子。我们发现,在IL-2刺激下,人蕈样真菌病(MF)肿瘤T细胞中的Gab2被酪氨酸短暂磷酸化,SHP2和Stat5a可诱导地与Gab2相关。IL-15而非IL-4也能诱导酪氨酸磷酸化Gab2,提示IL-2受体β链在IL-2诱导的Gab2磷酸化中起重要作用。用Src家族激酶抑制剂PP1预孵生的细胞,令人惊讶地增加了IL-2和il -15诱导的酪氨酸磷酸化的Gab2,这表明Src家族激酶成员负调控MF T细胞中的IL-2受体信号。因此,尽管与正常T细胞相比,Gab2在MF T细胞中似乎功能正常,但Gab2本身可能受到Src家族激酶的异常调节。
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Gab2 Is Phosphorylated on Tyrosine upon Interleukin-2/Interleukin-15 Stimulation in Mycosis-fungoides-Derived Tumor T Cells and Associates Inducibly with SHP-2 and Stat5a
Cutaneous T cell lymphomas (CTCLs) often show abnormal interleukin-2 (IL-2) receptor signaling. In this study, we investigated the role of Gab2, a recently identified adaptor molecule involved in IL-2 receptor signaling in CTCLs. We show that Gab2 was transiently phosphorylated by tyrosine in human mycosis fungoides (MF) tumor T cells upon IL-2 stimulation and that SHP2 as well as Stat5a associated inducibly with Gab2. IL-15, but not IL-4, also induced tyrosine phosphorylation of Gab2, suggesting that the IL-2 receptor β-chain is important for IL-2-induced Gab2 phosphorylation. Preincubation of cells with the Src family kinase inhibitor, PP1, surprisingly increased the IL-2- and IL-15-induced tyrosine phosphorylation of Gab2, indicating that an Src family kinase member negatively regulates IL-2 receptor signaling in MF T cells. Thus, although Gab2 seems to function normally in MF T cells compared to normal T cells, Gab2 itself might be abnormally regulated by an Src family kinase.
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