急性心肌梗死中自然杀伤细胞活性降低。
Depressed natural killer cell activity in acute myocardial infarction.
作者信息
Klarlund K, Pedersen B K, Theander T G, Andersen V
机构信息
Department of Cardiology, Copenhagen County Hospital, Gentofte, Denmark.
出版信息
Clin Exp Immunol. 1987 Oct;70(1):209-16.
Natural killer (NK) cell activity against K562 target cells was measured in patients within 24 h of acute myocardial infarction (AMI) and regularly thereafter for 6 weeks. NK cell activity was suppressed on days 1, 3, and 7 (P less than 0.01), day 14 (P less than 0.05) and at 6 weeks (P = 0.05) when compared to controls. Interferon, interleukin 2 and indomethacin enhanced NK cell activity on all days measured, but did not completely restore the defective NK cell activity. Serum from the patients did not suppress the NK cell activity of healthy mononuclear cells. The number of NK cells, identified as large granular lymphocytes (LGL), measured on days 1, 3, and 14 and at 6 weeks was not reduced in comparison to that of controls. Thus, the defective NK cell activity can be characterized as functional.
在急性心肌梗死（AMI）患者发病24小时内及其后6周内定期检测其针对K562靶细胞的自然杀伤（NK）细胞活性。与对照组相比，NK细胞活性在第1、3、7天（P<0.01）、第14天（P<0.05）和6周时（P = 0.05）受到抑制。在所有检测日，干扰素、白细胞介素2和吲哚美辛均可增强NK细胞活性，但不能完全恢复缺陷的NK细胞活性。患者血清并未抑制健康单核细胞的NK细胞活性。与对照组相比，在第1、3、14天和6周时检测到的被鉴定为大颗粒淋巴细胞（LGL）的NK细胞数量并未减少。因此，缺陷的NK细胞活性可被表征为功能性的。
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