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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Thymic stromal lymphopoietin-mediated STAT5 phosphorylation via kinases JAK1 and JAK2 reveals a key difference from IL-7-induced signaling
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Thymic stromal lymphopoietin-mediated STAT5 phosphorylation via kinases JAK1 and JAK2 reveals a key difference from IL-7-induced signaling

机译：胸腺基质淋巴细胞生成素通过激酶JAK1和JAK2介导的STAT5磷酸化揭示了与IL-7诱导的信号传导的关键区别

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摘要

Thymic stromal lymphopoietin (TSLP) is a type I cytokine that plays essential roles in allergic/inflammatory skin and airway disorders, in helminth infections, and in regulating intestinal immunity. TSLP signals via IL-7Rα and a specific TSLPR subunit that is highly related to the common cytokine receptor γ chain, γ_c. Although TSLP has effects on a broad range of hematopoetic cells and can induce STAT5 phosphorylation, TSLP was reported to not signal via JAK kinases, and the mechanism by which TSLP regulates STAT5 phosphorylation has been unclear. We now demonstrate the role of JAK1 and JAK2 in TSLP-mediated STAT5 phosphorylation in mouse and human primary CD4~+ T cells, in contrast to the known activation of JAK1 and JAK3 by the related cytokine, IL-7. We also show that just as JAK1 interacts with IL-7Rα, JAK2 is associated with TSLPR protein. Moreover, we demonstrate the importance of STAT5 activation for TSLP-mediated survival and proliferation of CD4~+ T cells. These findings clarify the basis for TSLP-mediated signaling and provide an example wherein a cytokine uses JAK1 and JAK2 to mediate the activation of STAT5.
机译：胸腺基质淋巴细胞生成素（TSLP）是I型细胞因子，在变应性/炎症性皮肤和气道疾病，蠕虫感染以及肠道免疫调节中起着重要作用。 TSLP通过IL-7Rα和与共同的细胞因子受体γ链γ_c高度相关的特定TSLPR亚基发出信号。尽管TSLP对广泛的造血细胞有影响并且可以诱导STAT5磷酸化，但是据报道TSLP不会通过JAK激酶发出信号，并且尚不清楚TSLP调节STAT5磷酸化的机制。现在我们证明JAK1和JAK2在TSLP介导的小鼠和人原代CD4〜+ T细胞中的STAT5磷酸化中的作用，这与相关细胞因子IL-7对JAK1和JAK3的激活作用相反。我们还显示，正如JAK1与IL-7Rα相互作用一样，JAK2与TSLPR蛋白相关。此外，我们证明了STAT5激活对于TSLP介导的CD4 + T细胞存活和增殖的重要性。这些发现阐明了TSLP介导的信号传导的基础，并提供了一个例子，其中细胞因子使用JAK1和JAK2介导STAT5的激活。

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    Yrina Rochman; Mohit Kashyap; Gertraud W. Robinson; Kazuhito Sakamoto; Julio Gomez-Rodriguez; Kay-Uwe Wagner; Warren J. Leonard;

  • 作者单位

    laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1674;

    laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1674;

    Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892;

    Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198-5950;

    Genetic Disease Research Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD 20892;

    Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198-5950;

    laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892-1674;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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