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MAGT1 介导的镁稳态紊乱导致 HBV 感染的 NK 和 CD8 T 细胞耗竭。

MAGT1-mediated disturbance of Mg homeostasis lead to exhausted of HBV-infected NK and CD8 T cells.

机构信息

Institute of Immunology, PLA, Third Military Medical University, Chongqing, China.

Magceutics, Inc, 3159 Corporate Place Hayward, California, 94545, USA.

出版信息

Sci Rep. 2017 Oct 19;7(1):13594. doi: 10.1038/s41598-017-11522-4.

Abstract

The magnesium transporter 1 (MAGT1) is a critical regulator of basal intracellular free magnesium ([Mg]i) levels. It has been shown that MAGT1 was involved in the disorder in Mg homeostasis after Epstein-Barr virus (EBV) infection. Here, we identified the effects of MAGT1-mediated disturbance of Mg homeostasis on chronic hepatitis B virus (HBV)-infected natural killer (NK) and CD8 T cells. The expression of MAGT1 was gradually decreased with the increase of infected time in CD8 T cells, but not with that in NK cells, of the patients. Decreased level of intracellular free Mg ([Mg]i) leads to defective expression of programmed cell death 1 (PD-1) and the NK activating receptor (NKG2D) in NK and CD8 T cells. Our data illustrate that [Mg]i plays a key role in control of HBV infection.

摘要

镁转运蛋白 1(MAGT1)是基础细胞内游离镁离子([Mg]i)水平的关键调节因子。有研究表明,MAGT1 参与了 EBV 感染后镁稳态紊乱。在此,我们研究了 MAGT1 介导的镁稳态紊乱对慢性 HBV 感染的自然杀伤(NK)和 CD8 T 细胞的影响。患者 CD8 T 细胞中 MAGT1 的表达随感染时间的增加而逐渐降低,但 NK 细胞中并非如此。细胞内游离镁([Mg]i)水平的降低导致 NK 和 CD8 T 细胞中程序性细胞死亡蛋白 1(PD-1)和 NK 激活受体(NKG2D)的表达缺陷。我们的数据表明,[Mg]i 在控制 HBV 感染中起着关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b546/5648775/1a1cab41aeb5/41598_2017_11522_Fig1_HTML.jpg

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