Objective: To test NK cell quantities and function in patients with positive BMMNC-Coombs test (CBCPC) and cytopenia and to explore how NK cell participate in the progress of this disease.
Methods: The percentage of CD3(-)CD56(+) NK cell in peripheral blood lymphocytes, the expression of activating receptor (NKG2D, NKp46, NKp44), inhibitory receptor (CD158a, CD158b), perforin and granzyme-β were detected by flow cytometry. All samples were taken from 42 patients (22 newly diagnosed and 20 in remission) and 12 healthy volunteers. The correlation between the above parameters and patients' clinical profile were evaluated.
Results: ①The percentage of CD3(-)CD56(+) NK cell in new diagnosed and remission CBCPC patients were significantly lower than that in healthy control [(10.04 ± 5.33)% vs (19.94 ± 7.38)%; (11.62 ± 6.80)% vs (19.94 ± 7.38)%, all P<0.01]. ② The expression of activating receptor NKG2D in new diagnosed CBCPC patients was significantly higher than that in remission group and healthy control [(74.03±18.24)% vs (45.97±29.45)%; (74.03±18.24)% vs (41.89± 15.34)% , P <0.01]. ③The expression of inhibitory receptor CD158a in new diagnosed CBCPC patients was significantly lower than that in remission group and healthy control (median: 3.72% vs 16.10%, P= 0.015; 3.72% vs 11.04%, P=0.025). ④The expression of perforin in new diagnosed and remitted CBCPC patients were significantly higher than that in healthy controls [(75.71±10.14) % vs (57.20±18.85)%, P= 0.018; (77.88±22.82)% vs (57.20±18.85)%, P=0.008]. ⑤The product of NK cell percentage and perforin expression in new diagnosed and remission CBCPC patient were significantly lower than that in healthy control [(7.68±4.54)% vs (12.13±5.19)%, P=0.011; (8.24±5.80)% vs (12.13±5.19)%, P=0.023]. The product of NK cell percentage and granzyme-β expression in the new diagnosed and remission CBCPC patient were significantly lower than that in healthy control [(7.83±5.26)% vs (14.79±8.37)%, P=0.008; (8.37 ± 6.83)% vs (14.79±8.37)%, P=0.012].
Conclusion: Deceased quantities and impaired total NK function might play a role in pathogenesis of CBCPC.
目的: 检测骨髓单个核细胞Coombs试验阳性血细胞减少症（CBCPC）患者外周血NK细胞数量和功能，探讨NK细胞在CBCPC发病中的作用机制。
方法: 采用流式细胞术检测20例CBCPC初治患者、22例CBCPC缓解患者和12名健康志愿者外周血NK细胞及其亚群比例，表面激活性受体NKG2D、NKp46、NKp44，抑制性受体CD158a、CD158b及穿孔素、颗粒酶β的表达。
结果: ①初治组、缓解组患者CD3−CD56+ NK细胞比例显著低于对照组[分别为（10.04±5.33）%、（11.62±6.80）%、（19.94±7.38）%，P值均<0.01]。②初治患者NK细胞激活性受体NKG2D比例（74.03±18.24）％显著高于缓解组患者[（45.97±29.45）%]和对照组[（41.89±15.34）%]（P值均<0.01）。③初治患者NK细胞抑制性受体CD158a中位水平为3.72%（7.88%），显著低于缓解组的16.10%（26.43%）和对照组的11.04%（22.87%）（P值分别为0.015、0.025）。④初治、缓解患者NK细胞穿孔素比例分别为（75.71±10.14）%、（77.88±22.82）%，均显著高于对照组的（60.22±14.58）%（P值分别为0.018、0.008）。⑤初治和缓解患者NK细胞比例与穿孔素比例乘积分别为（7.68±4.54）%、（8.24±5.80）%，均显著低于对照组的（12.13±5.19）%（P值分别为0.011、0.023）；初治和缓解患者NK细胞比例与颗粒酶β比例乘积分别为（7.83±5.26）%、（8.37±6.83）％显著低于对照组的（14.79±8.37）%（P值分别为0.008、0.012）。
结论: 初治CBCPC患者NK细胞比例降低，激活性受体表达增加，抑制性受体表达降低，提示NK细胞在CBCPC发病机制中起保护作用，但代偿不足。