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Up-regulation of NKG2A Inhibitory Receptor on Circulating NK Cells Contributes to Transfusion-induced Immunodepression in Patients with β-thalassemia Major

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 e...

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Published in:Journal of Huazhong University of Science and Technology. Medical sciences 2016-08, Vol.36 (4), p.509-513
Main Author: 邹勇 宋志兴 陆英 梁晓莉 袁青 廖思红 鲍俊杰
Format: Article
Language:English
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Summary: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, CD158 a, NKP30, NKP46 and NKG2D) as well as CD107 a 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 NKG2 A 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, NKG2 D, CD158 a and IFN-γ. These results indicate NKG2 A inhibitory receptor may play a key role in transfusion-induced immunodepression of NK cells in patients with β-thalassemia major.
ISSN:1672-0733
1993-1352
DOI:10.1007/s11596-016-1616-5