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由于自然杀伤细胞增多,体外补充锌可增强1型辅助性T细胞因子的释放。

T-helper type 1 cytokine release is enhanced by in vitro zinc supplementation due to increased natural killer cells.

作者信息

Metz Claudia H D, Schröder Anja K, Overbeck Silke, Kahmann Laura, Plümäkers Birgit, Rink Lothar

机构信息

Institute of Immunology, RWTH Aachen University Hospital, Aachen, Germany.

出版信息

Nutrition. 2007 Feb;23(2):157-63. doi: 10.1016/j.nut.2006.10.007. Epub 2006 Dec 5.

DOI:10.1016/j.nut.2006.10.007
PMID:17150331
Abstract

OBJECTIVE

We examined the influence of zinc on T-helper type 1 (Th1)/T-helper type 2 (Th2) balance in human lymphocytes.

METHODS

Human peripheral blood mononuclear cells or diluted whole blood were cultured for 8 d in the presence of zinc (30 or 60 microM) or 1 microM of N, N, N', N'-tetrakis(2-pyridylmethyl)ethylenediamine (TPEN) (a zinc-specific chelator). Phytohemagglutinin-induced cytokine release was measured by enzyme-linked immunosorbent assay, and expression of CD56/CD69, CCR4/CD3, and CCR5/CD3 and intracellular labile zinc were detected by flow cytometry.

RESULTS

We found that our in vitro supplementation resulted in an increase of intracellular labile zinc comparable to that of a 7-wk administration of 10 mg of zinc per day in vivo. Zinc triggered interferon-gamma release and impaired interleukin-10 release. Phenotypically, a Th2/Th1 shift could not be confirmed after detecting the Th1-specific chemokine receptor CCR5 or CCR4 for Th2 cells. Surprisingly, we detected a larger amount of CD56+ cells after zinc stimulation, leading us to the conclusion that the amount of interferon-gamma release after zinc supplementation might be attributed to the upregulation of natural killer cells after in vitro zinc supplementation rather than to a Th2/Th1 shift.

CONCLUSION

We suggest that a nutritional intake of 10 mg of zinc increases the quantity of interferon-gamma-producing natural killer cells and strengthens the immune system against neoplasms and viral infections.

摘要

目的

我们研究了锌对人淋巴细胞中1型辅助性T细胞(Th1)/2型辅助性T细胞(Th2)平衡的影响。

方法

将人外周血单个核细胞或稀释的全血在锌(30或60微摩尔)或1微摩尔的N,N,N',N'-四(2-吡啶甲基)乙二胺(TPEN)(一种锌特异性螯合剂)存在下培养8天。通过酶联免疫吸附测定法测量植物血凝素诱导的细胞因子释放,并通过流式细胞术检测CD56/CD69、CCR4/CD3和CCR5/CD3的表达以及细胞内不稳定锌。

结果

我们发现,我们的体外补充导致细胞内不稳定锌增加,这与体内每天服用10毫克锌7周的效果相当。锌引发γ干扰素释放并损害白细胞介素-10释放。在检测Th2细胞的Th1特异性趋化因子受体CCR5或CCR4后,未能从表型上证实Th2/Th1转变。令人惊讶的是,我们在锌刺激后检测到大量CD56+细胞,这使我们得出结论,锌补充后γ干扰素释放量可能归因于体外锌补充后自然杀伤细胞的上调,而不是Th2/Th1转变。

结论

我们认为,摄入10毫克锌可增加产生γ干扰素的自然杀伤细胞数量,并增强免疫系统抵抗肿瘤和病毒感染的能力。

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