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循环自然杀伤细胞上NKG2A抑制性受体的上调促成了重型β地中海贫血患者输血诱导的免疫抑制。

Up-regulation of NKG2A inhibitory receptor on circulating NK cells contributes to transfusion-induced immunodepression in patients with β-thalassemia major.

作者信息

Zou Yong, Song Zhi-Xing, Lu Ying, Liang Xiao-Li, Yuan Qing, Liao Si-Hong, Bao Jun-Jie

机构信息

Department of Blood Transfusion, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, China.

Department of Clinical Laboratory, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, 510630, China.

出版信息

J Huazhong Univ Sci Technolog Med Sci. 2016 Aug;36(4):509-513. doi: 10.1007/s11596-016-1616-5. Epub 2016 Jul 28.

DOI:10.1007/s11596-016-1616-5
PMID:27465324
Abstract

Accumulating evidence has shown that allogeneic blood transfusions can induce significant immunosuppression in recipients, and thereby increase the risk of postoperative infection and/or tumor relapse. Although it is well known that natural killer (NK) cells are responsible for the immunodepression effects of transfusion, the underlying mechanisms remain obscure. In this study, we investigated the role of NK cells in transfusion-induced immunodepression in β-thalassemia major. The proportion of circulating NK cells and the expression of NK receptors (NKG2A, CD158a, NKP30, NKP46 and NKG2D) as well as CD107a were detected by multicolor flow cytometry. IFN-γ production by circulating NK cells was detected by intracellular cytokine staining. Our results showed that the proportion and cytotoxicity (CD107a expression) of circulating NK cells in transfusion-dependent β-thalassemia major patients were remarkably lower than those of β-thalassemia minor patients or healthy volunteers. Expression of NKG2A inhibitory receptor on circulating NK cells in patients with β-thalassemia major was remarkably up-regulated, but there were no significant differences in the expression levels of NKP30, NKP46, NKG2D, CD158a and IFN-γ. These results indicate NKG2A inhibitory receptor may play a key role in transfusion-induced immunodepression of NK cells in patients with β-thalassemia major.

摘要

越来越多的证据表明,异体输血可诱导受血者产生显著的免疫抑制,从而增加术后感染和/或肿瘤复发的风险。虽然众所周知自然杀伤(NK)细胞是输血免疫抑制作用的原因,但潜在机制仍不清楚。在本研究中,我们调查了NK细胞在重型β地中海贫血输血诱导的免疫抑制中的作用。通过多色流式细胞术检测循环NK细胞的比例、NK受体(NKG2A、CD158a、NKP30、NKP46和NKG2D)以及CD107a的表达。通过细胞内细胞因子染色检测循环NK细胞产生的IFN-γ。我们的结果显示,依赖输血的重型β地中海贫血患者循环NK细胞的比例和细胞毒性(CD107a表达)明显低于轻型β地中海贫血患者或健康志愿者。重型β地中海贫血患者循环NK细胞上NKG2A抑制性受体的表达明显上调,但NKP30、NKP46、NKG2D、CD158a和IFN-γ的表达水平没有显著差异。这些结果表明,NKG2A抑制性受体可能在重型β地中海贫血患者输血诱导的NK细胞免疫抑制中起关键作用。

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本文引用的文献

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