Second messenger role for Mg~(2+) revealed by human T-cell immunodeficiency

Feng-Yen Li; Benjamin Chaigne-Delalande; Chrysi Kanellopoulou; Jeremiah C. Davis; Helen F. Matthews; Daniel C. Douek; Jeffrey I. Cohen; Gulbu Uzel; Helen C. Su; Michael J. Lenardo

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Second messenger role for Mg~(2+) revealed by human T-cell immunodeficiency

机译：人类T细胞免疫缺陷揭示Mg〜（2+）的第二信使作用

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The magnesium ion, Mg~(2+1), is essential for all life as a cofactor for ATP, polyphosphates such as DNA and RNA, and metabolic enzymes, but whether it plays a part in intracellular signalling (as Ca~(2+) does) is unknown. Here we identify mutations in the magnesium transporter gene, MAGT1, in a novel X-linked human immunodeficiency characterized by CD4 lymphopenia, severe chronic viral infections, and defective T-lymphocyte activation. We demonstrate that a rapid transient Mg~(2+1) influx is induced by antigen receptor stimulation in normal T cells and by growth factor stimulation in non-lymphoid cells. MAGT1 deficiency abrogates the Mg~(2+1) influx, leading to impaired responses to antigen receptor engagement, including defective activation of phospholipase Cyl and a markedly impaired Mg~(2+1) influx in T cells but not B cells. These observations reveal a role for Mg~(2+1) as an intracellular second messenger coupling cell-surface receptor activation to intracellular effectors and identify MAGT1 as a possible target for novel therapeutics.

机译：镁离子Mg〜（2 + 1）作为ATP，DNA和RNA等多磷酸盐和代谢酶的辅助因子，对于生命中至关重要，但镁离子是否参与细胞内信号传导（如Ca〜（2+ ）确实）是未知的。在这里，我们在以X4连锁的人类免疫缺陷为特征的CD4淋巴细胞减少症，严重的慢性病毒感染和有缺陷的T淋巴细胞活化中，鉴定了镁转运蛋白MAGT1中的突变。我们证明快速瞬态Mg〜（2 + 1）涌入是由正常T细胞中的抗原受体刺激和非淋巴细胞中的生长因子刺激引起的。 MAGT1缺乏消除了Mg〜（2 + 1）流入，导致对抗原受体参与的反应受损，包括磷脂酶Cyl的激活缺陷，而T细胞而非B细胞中的Mg〜（2 + 1）流入明显受损。这些观察结果揭示了Mg〜（2 + 1）作为将细胞表面受体激活偶联至细胞内效应子的细胞内第二信使的作用，并将MAGT1鉴定为新疗法的可能靶标。

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《Nature》 |2011年第7357期|p.471-476|共6页
作者
Feng-Yen Li; Benjamin Chaigne-Delalande; Chrysi Kanellopoulou; Jeremiah C. Davis; Helen F. Matthews; Daniel C. Douek; Jeffrey I. Cohen; Gulbu Uzel; Helen C. Su; Michael J. Lenardo;
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作者单位

Molecular Development Section, Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA,Biomedical Sciences Graduate Program, University of California-San Francisco, San Francisco, California 94143, USA;

Molecular Development Section, Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

Molecular Development Section, Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

Human Immunological Diseases Unit, Laboratory of Host Defenses,National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

Molecular Development Section, Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

Human Immunology Section, Vaccine Research Center, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health,Bethesda, Maryland 20892, USA;

Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

Human Immunological Diseases Unit, Laboratory of Host Defenses,National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

Molecular Development Section, Lymphocyte Molecular Genetics Unit, Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA;

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收录信息美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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Second messenger role for Mg~(2+) revealed by human T-cell immunodeficiency

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