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在慢性乙型肝炎患者外周血T淋巴细胞中观察到细胞凋亡。

Apoptosis observed in peripheral T lymphocytes from patients with chronic hepatitis B.

作者信息

Nakamura K, Yuh K, Sugyo S, Shijo H, Kimura N, Okumura M

机构信息

First Department of Internal Medicine, School of Medicine, Fukuoka University, Japan.

出版信息

Gastroenterology. 1996 Jul;111(1):156-64. doi: 10.1053/gast.1996.v111.pm8698194.

DOI:10.1053/gast.1996.v111.pm8698194
PMID:8698194
Abstract

BACKGROUND & AIMS: Activation-induced cell death is involved in regulating peripheral T-cell function. Understanding the kinetics of these T cells is important to elucidate the pathogenesis of chronic hepatitis B, which is mediated by cellular immune mechanisms.

METHODS

Subtle apoptotic cells in CD3+ cells were discriminated by flow-cytometric assay using freshly obtained and in vitro recombinant hepatitis B core antigen-stimulated peripheral lymphocytes from patients with chronic hepatitis.

RESULTS

The ratio of apoptotic cells in freshly obtained CD3+ cells was significantly higher during the decreasing phase than increasing phase of serum alanine aminotransferase activity in each patient, and apoptosis of CD3+ cells was induced by stimulation with recombinant hepatitis B core antigen.

CONCLUSIONS

Activation-induced cell death in peripheral T cells was found in chronic hepatitis B virus infection, similar to some other viral infections. The apoptosis in T cells during the decreasing phase of serum alanine aminotransferase activity results in a vast amount of T-cell deletion that may weaken T-cell function of cytotoxicity over hepatitis B virus-infected hepatocytes. Thus, activation-induced cell death is considered an important modulator in down-regulating the "burst" of responding T cells in patients with chronic hepatitis B.

摘要

背景与目的

活化诱导的细胞死亡参与调节外周T细胞功能。了解这些T细胞的动力学对于阐明由细胞免疫机制介导的慢性乙型肝炎的发病机制很重要。

方法

使用从慢性肝炎患者新鲜获取的以及体外重组乙肝核心抗原刺激的外周淋巴细胞,通过流式细胞术检测区分CD3⁺细胞中的细微凋亡细胞。

结果

在每位患者中,血清丙氨酸氨基转移酶活性下降期新鲜获取的CD3⁺细胞中凋亡细胞的比例显著高于上升期,并且重组乙肝核心抗原刺激可诱导CD3⁺细胞凋亡。

结论

在慢性乙型肝炎病毒感染中发现外周T细胞存在活化诱导的细胞死亡,这与其他一些病毒感染类似。血清丙氨酸氨基转移酶活性下降期T细胞凋亡导致大量T细胞缺失,这可能会削弱针对乙肝病毒感染肝细胞的细胞毒性T细胞功能。因此,活化诱导的细胞死亡被认为是下调慢性乙型肝炎患者反应性T细胞“爆发”的重要调节因子。

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