SLC39A6/ZIP6 is essential for zinc homeostasis and T-cell development in zebrafish
SLC39A6/ZIP6 is essential for zinc homeostasis and T-cell development in zebrafish
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SLC39A6/ZIP6 对于斑马鱼的锌稳态和 T 细胞发育至关重要
DOI：
10.1016/j.bbrc.2019.02.148
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发表时间：
2019
影响因子：
3.1
通讯作者：
Zhou Jianfeng
中科院分区：
文献类型：
--
作者：
Zhao Lei;Tan Jiaqi;Li Dan;Jiang Lijun;Li Tongjuan;Yang Yi;Wang Gaoxiang;Shang Zhen;Wang Jue;Zhou Jianfeng
锌（Zn）是调节先天性和获得性免疫反应的必需微量元素，其缺乏会引发淋巴细胞减少症。然而，锌介导的淋巴细胞维持的确切机制尚未得到很好的阐明。在这里，我们已经使用TALEN成功地产生了azip 6-null突变体斑马鱼系。Zip 6缺失突变体斑马鱼在原肠胚形成过程中发育正常。zip 6基因缺失导致斑马鱼T淋巴细胞数量显著减少，细胞内锌水平降低。zip 6缺陷增加了斑马鱼细胞和人类T细胞中与半胱天冬酶相关的细胞凋亡。我们的研究结果表明，ZIP 6在T细胞发育中起着关键作用，并增强了我们对锌稳态和免疫系统维护的理解。
Zinc (Zn) is an essential trace element that modulate innate and acquired immune responses, and its deficiency triggers lymphopenia. However, the precise mechanisms underlying zinc-mediated lymphocyte maintenance have not been well clarified. Here, we have successfully generated azip6-null mutant zebrafish line using TALENs. TheZip6-null mutant zebrafish developed normally during gastrulation. Loss ofzip6in zebrafish resulted in significant T lymphocyte reduction and a decrease in intracellular Zn levels. And thezip6deficiency increases caspase-related cell apoptosis in both zebrafish cells and human T cells. Our results suggest thatZIP6plays a critical part in T cell development, and enhance our understanding of Zn homeostasis and immune system maintenance.