骨髓单个核细胞Coombs试验阳性血细胞减少症患者NK细胞数量及功能研究

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]. ②The 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.