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非重型再生障碍性贫血中CD56bright自然杀伤细胞数量及功能异常

Abnormalities of quantities and functions of CD56bright natural killer cells in non-severe aplastic Anemia.

作者信息

Li Yang, Ding Shaoxue, Liu Chunyan, Chen Tong, Liu Hui, Li Lijuan, Shao Zonghong, Fu Rong

出版信息

Hematology. 2019 Dec;24(1):405-412. doi: 10.1080/16078454.2019.1590963.

DOI:10.1080/16078454.2019.1590963
PMID:30907293
Abstract

OBJECTIVES

The mechanism of non-severe aplastic anemia (NSAA) is not clear. It may be different from severe aplastic anemia (SAA). CD56bright NK cells (regulatory NK cells) is a subgroup of NK cells that produce immunoregulatory cytokines and express high-affinity IL-2 receptor. To investigate CD56bright NK cells quantities and function in patients with NSAA and to explore how CD56bright NK cells participate in the progress of this disease.

METHODS

In this study, we analyzed the quantitative and functional changes of CD56bright NK cells in peripheral blood of patients with NSAA by using Flow Cytometry (FCM) before and after immunosuppressive therapy (IST). The expressions of activating receptor (NKG2D, NKp46, NKp44), inhibitory receptor (NKG2A, CD158a, CD158b) and perforin and granzyme B were detected by FCM. IL-2 and IL-18 levels in serum were detected by ELISA. The correlation between these parameters and clinical indicators of patients were evaluated.

RESULTS

We found that the percentage of CD56bright NK cells in newly diagnosed NSAA patients was higher than that in normal controls (p = .011, p < .05). The median expression of NKG2D in patients with NSAA was higher compared to that in normal controls (p = .021, p < .05), and the expression of CD158a was lower (p = .047, p < .05). The concentrations of IL-2 and IL-18 in the serum of patients with NSAA were higher than those in normal group.

CONCLUSION

These findings suggest that increased and activated CD56bright NK cells might play a protective role in the pathogenesis of NSAA.

摘要

目的

非重型再生障碍性贫血(NSAA)的发病机制尚不清楚。其机制可能与重型再生障碍性贫血(SAA)不同。CD56bright自然杀伤细胞(调节性自然杀伤细胞)是自然杀伤细胞的一个亚群,可产生免疫调节细胞因子并表达高亲和力白细胞介素-2受体。旨在研究NSAA患者中CD56bright自然杀伤细胞的数量和功能,并探讨CD56bright自然杀伤细胞如何参与该疾病的进展。

方法

在本研究中,我们采用流式细胞术(FCM)分析了免疫抑制治疗(IST)前后NSAA患者外周血中CD56bright自然杀伤细胞的数量和功能变化。通过FCM检测活化受体(NKG2D、NKp46、NKp44)、抑制性受体(NKG2A、CD158a、CD158b)以及穿孔素和颗粒酶B的表达。采用酶联免疫吸附测定法(ELISA)检测血清中白细胞介素-2和白细胞介素-18水平。评估这些参数与患者临床指标之间的相关性。

结果

我们发现新诊断的NSAA患者中CD56bright自然杀伤细胞的百分比高于正常对照组(p = 0.011,p < 0.05)。NSAA患者中NKG2D的中位表达高于正常对照组(p = 0.021,p < 0.05),而CD158a的表达较低(p = 0.047,p < 0.05)。NSAA患者血清中白细胞介素-2和白细胞介素-18的浓度高于正常组。

结论

这些发现表明,CD56bright自然杀伤细胞的增加和活化可能在NSAA的发病机制中起保护作用。

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