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白细胞介素-18增强肝脏自然杀伤T细胞的穿孔素依赖性细胞毒性。

IL-18 augments perforin-dependent cytotoxicity of liver NK-T cells.

作者信息

Dao T, Mehal W Z, Crispe I N

机构信息

Immunobiology Section, Yale University School of Medicine, New Haven, CT 06520, USA.

出版信息

J Immunol. 1998 Sep 1;161(5):2217-22.

PMID:9725214
Abstract

The liver contains abundant cytotoxic cells, including NK-T cells, NK cells, and CTLs. However, the regulation of this cytotoxicity is not fully understood. In this study, we investigated the effect of a recently described cytokine, IL-18, which is present in large quantities in the liver, on the cytotoxicity of intrahepatic lymphocyte subpopulations. This effect of IL-18 was assessed by assaying the in vitro cytotoxicity of purified NK-T, NK, and T cells against a CD95- and perforin-sensitive T cell line, Jurkat. The results show that IL-18 enhances the killing activity of liver NK-T cells by a CD95-independent, perforin-dependent pathway. IL-18 also augments liver NK cell activity, but the exact mechanisms of this killing remain to be elucidated. Finally, the augmentation of the killing activities of liver NK-T and NK cells by IL-18 is not due to soluble TNF-alpha, because none of these cell populations had detectable TNF-alpha production.

摘要

肝脏含有丰富的细胞毒性细胞,包括自然杀伤T细胞、自然杀伤细胞和细胞毒性T淋巴细胞。然而,这种细胞毒性的调节机制尚未完全明确。在本研究中,我们调查了一种最近被描述的细胞因子白细胞介素-18(IL-18)对肝内淋巴细胞亚群细胞毒性的影响,IL-18在肝脏中大量存在。通过检测纯化的自然杀伤T细胞、自然杀伤细胞和T细胞对CD95和穿孔素敏感的T细胞系Jurkat的体外细胞毒性,评估了IL-18的这种作用。结果显示,IL-18通过一条不依赖CD95、依赖穿孔素的途径增强肝脏自然杀伤T细胞的杀伤活性。IL-18也增强肝脏自然杀伤细胞的活性,但这种杀伤的确切机制仍有待阐明。最后,IL-18增强肝脏自然杀伤T细胞和自然杀伤细胞的杀伤活性并非由于可溶性肿瘤坏死因子-α,因为这些细胞群体均未检测到肿瘤坏死因子-α的产生。

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