Abnormalities of quantities and functions of CD56bright natural killer cells in non-severe aplastic Anemia
Abnormalities of quantities and functions of CD56bright natural killer cells in non-severe aplastic Anemia
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非重症再生障碍性贫血CD56bright自然杀伤细胞数量及功能异常
DOI：
10.1080/16078454.2019.1590963
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发表时间：
2019-01-01
期刊：
影响因子：
1.9
通讯作者：
Fu, Rong
中科院分区：
文献类型：
--
作者：
Li, Yang;Ding, Shaoxue;Fu, Rong
【摘要】目的非重度再生障碍性贫血（NSAA）的发病机制尚不清楚。它可能不同于严重再生障碍性贫血（SAA）。CD56bright NK细胞（调节性NK细胞）是NK细胞的一个亚群，产生免疫调节性细胞因子，表达高亲和力IL-2受体。研究NSAA患者中CD56bright NK细胞的数量和功能，探讨CD56bright NK细胞如何参与该疾病的进展。方法采用流式细胞术（FCM）分析免疫抑制治疗（IST）前后NSAA患者外周血CD56bright NK细胞的数量和功能变化。流式细胞术检测激活受体（NKG2D、NKp46、NKp44）、抑制受体（NKG2A、CD158a、CD158b）、穿孔素和颗粒酶B的表达。ELISA法检测血清中IL-2、IL-18水平。评价这些参数与患者临床指标的相关性。结果我们发现新诊断的NSAA患者中CD56bright NK细胞的百分比高于正常对照组(p =。011, p < 0.05)。NKG2D在NSAA患者中的中位表达量高于正常对照组(p =。021, p <。CD158a表达较低（p = 0.05）， CD158a表达较低（p = 0.05）。047, p < 0.05)。NSAA患者血清中IL-2、IL-18浓度明显高于正常组。结论CD56bright NK细胞的增加和活化可能在NSAA的发病机制中起保护作用。
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.