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急性乙型肝炎中的白细胞介素-2与自然杀伤活性

Interleukin-2 and natural killer activity in acute type B hepatitis.

作者信息

Echevarria S, Casafont F, Miera M, Lozano J L, de la Cruz F, San Miguel G, Pons Romero F

机构信息

Department of Internal Medicine, H.N. Marqués de Valdecilla, Faculty of Medicine, Santander, Spain.

出版信息

Hepatogastroenterology. 1991 Aug;38(4):307-10.

PMID:1937376
Abstract

Natural killer (NK) cell activity against K562 cell line, and interleukin-2 (IL-2) activity in supernatants from lectin-activated PBMC cultures from 17 patients with acute hepatitis B in the early phase of illness were studied. These patients showed enhanced NK cytotoxicity and higher levels of IL2 activity as compared with control subjects. There was a positive correlation between cytotoxicity values and levels of IL2 activity. Furthermore, in the recovery phase of illness there was a tendency towards normalization in both parameters. When patients were divided in accordance with markers of HBV replication, HBV-DNA positive patients showed increased NK cell activity and IL2 levels as compared with the control group, whereas in HBV-DNA-negative patients no differences were found. However, no differences were found between patients with HBeAg and patients with anti-HBe. These results suggest that natural cytotoxicity is increased early in the course of acute hepatitis B, while NK cell activity returns to normal later, during convalescence. Enhanced NK cell activity appears to be secondary, at least in part, to increased production of IL2. Natural cytotoxicity may be one mechanism that controls the HBV infection before other cytotoxic mechanisms become fully operative.

摘要

研究了17例急性乙型肝炎患者疾病早期针对K562细胞系的自然杀伤(NK)细胞活性,以及来自凝集素激活的外周血单核细胞(PBMC)培养上清液中的白细胞介素-2(IL-2)活性。与对照受试者相比,这些患者表现出增强的NK细胞毒性和更高水平的IL-2活性。细胞毒性值与IL-2活性水平之间呈正相关。此外,在疾病恢复期,这两个参数都有趋于正常的趋势。当根据HBV复制标志物对患者进行分组时,与对照组相比,HBV-DNA阳性患者的NK细胞活性和IL-2水平升高,而HBV-DNA阴性患者未发现差异。然而,HBeAg阳性患者与抗-HBe阳性患者之间未发现差异。这些结果表明,在急性乙型肝炎病程早期自然细胞毒性增加,而NK细胞活性在恢复期后期恢复正常。增强的NK细胞活性似乎至少部分是IL-2产生增加的继发结果。自然细胞毒性可能是在其他细胞毒性机制完全起作用之前控制HBV感染的一种机制。

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