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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Differential effects of STAT5 and PI3K/AKT signaling on effector and memory CD8 T-cell survival
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Differential effects of STAT5 and PI3K/AKT signaling on effector and memory CD8 T-cell survival

机译：STAT5和PI3K / AKT信号转导对效应子和记忆CD8 T细胞存活的差异作用

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摘要

During viral infection, effector CD8 T cells contract to form a population of protective memory cells that is maintained by IL-7 and IL-15. The mechanisms that control effector cell death during infection are poorly understood. We investigated how short- and long-lived antiviral CD8 T cells differentially used the survival and cell growth pathways PI3K/AKT and JAK/STAT5. In response to IL-15, long-lived memory precursor cells activated AKT significantly better than shortlived effector cells. However, constitutive AKT activation did not enhance memory CD8 T-cell survival but rather repressed IL-7 and IL-15 receptor expression, STAT5 phosphorylation, and BCL2 expression. Conversely, constitutive STAT5 activation profoundly enhanced effector and memory CD8 T-cell survival and augmented homeostatic proliferation, AKT activation, and BCL2 expression. Taken together, these data illustrate that effector and memory cell viability depends on properly balanced PI3K/AKT signaling and the maintenance of STAT5 signaling.
机译：在病毒感染期间，效应器CD8 T细胞收缩形成一群保护性记忆细胞，这些细胞由IL-7和IL-15维持。在感染过程中控制效应细胞死亡的机制了解甚少。我们研究了短寿命和长寿命的抗病毒CD8 T细胞如何差异性地利用存活和细胞生长途径PI3K / AKT和JAK / STAT5。响应IL-15，长寿命记忆前体细胞激活AKT的效果明显好于短时效应细胞。但是，本构性AKT激活并不能提高CD8 T细胞记忆的存活率，而是抑制IL-7和IL-15受体的表达，STAT5磷酸化和BCL2的表达。相反，组成型STAT5激活可显着增强效应子和记忆CD8 T细胞的存活，并增加体内稳态增殖，AKT激活和BCL2表达。总而言之，这些数据说明了效应子和记忆细胞的生存能力取决于适当平衡的PI3K / AKT信号传导和STAT5信号传导的维持。

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    Timothy W. Hand; Weiguo Cui; Yong Woo Jung; Esen Sefik; Nikhil S. Joshi; Anmol Chandele; Ying Liu; Susan M. Kaech;

  • 作者单位

    Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;

    rnDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;

    rnDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;

    rnDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;

    rnDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;

    rnDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;

    rnDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520;

    rnDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520 Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520;

  • 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);
  • 原文格式 PDF
  • 正文语种 eng
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  • 关键词

    apoptosis; cytokine signaling; interleukin 15; interleukin 7'; lymphocytic choriomeningitis virus;

    机译：细胞凋亡细胞因子信号;白介素15;白介素7';淋巴细胞性脉络膜脑膜炎病毒;

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