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肝细胞癌患者中抑郁的淋巴因子激活的杀伤细胞活性增强。

Enhancement of depressed lymphokine activated killer cell activity in patients with hepatocellular carcinoma.

作者信息

Saibara T, Onishi S, Matsuura Y, Fujikawa M, Sakaeda H, Matsunaga Y, Yamamoto Y

机构信息

First Department of Medicine, Kochi Medical School, Japan.

出版信息

Biotherapy. 1990;2(1):1-12. doi: 10.1007/BF02172071.

DOI:10.1007/BF02172071
PMID:2169282
Abstract

Hepatocellular carcinoma (HCC) patients can be divided into two groups according to the degree of lymphokine activated killer (LAK) cell activity; a high LAK activity group (H-LAK-HCC) and a low LAK activity group (L-LAK-HCC). Interferon-gamma (IFN-gamma) production is severely defective in L-LAK-HCC but not defective in H-LAH-HCC. IFN-gamma production is suppressed with the addition of anti-Tac in dose dependent manner, though LAK activity is suppressed only in the presence of high concentration of anti-Tac. LAK activity is suppressed with the addition of anti-IFN-gamma, which is most prominent when the antibody is present during the first 12 hr of incubation. LAK generation is enhanced with the addition of recombinant IFN-gamma, which is most prominent when it is present during the first 12 hr of incubation. However, this enhancing effect is less prominent in L-LAK-HCC as compared to normals, liver cirrhosis, and H-LAK-HCC. This enhancement is regarded to depend on the presence of Leu7+ and Leu11+ subset, as this enhancement is abandoned and IFN-gamma production is inhibited when either of these subsets is deleted. These data suggest that IFN-gamma production and the participation of Leu7+ and Leu11+ subsets is important in sufficient LAK generation, and that poor IFN-gamma production and insufficient response to IFN-gamma may be the cause of severely defective LAK generation in L-LAK-HCC.

摘要

肝细胞癌(HCC)患者可根据淋巴因子激活的杀伤细胞(LAK)活性程度分为两组;高LAK活性组(H-LAK-HCC)和低LAK活性组(L-LAK-HCC)。γ干扰素(IFN-γ)的产生在L-LAK-HCC中严重缺陷,但在H-LAH-HCC中无缺陷。添加抗Tac后,IFN-γ的产生以剂量依赖方式受到抑制,尽管只有在高浓度抗Tac存在时LAK活性才受到抑制。添加抗IFN-γ后LAK活性受到抑制,当抗体在孵育的前12小时存在时这种抑制最为明显。添加重组IFN-γ可增强LAK的产生,当它在孵育的前12小时存在时这种增强最为明显。然而,与正常、肝硬化和H-LAK-HCC相比,这种增强作用在L-LAK-HCC中不太明显。这种增强被认为取决于Leu7+和Leu11+亚群的存在,因为当这些亚群中的任何一个被删除时,这种增强作用就会消失且IFN-γ的产生会受到抑制。这些数据表明,IFN-γ的产生以及Leu7+和Leu11+亚群的参与对于充分产生LAK很重要,并且IFN-γ产生不足和对IFN-γ反应不足可能是L-LAK-HCC中LAK产生严重缺陷的原因。

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