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蛋白结合多糖(PSK)对胃癌患者外周血、区域淋巴结及脾脏淋巴细胞的体外免疫调节作用。

In vitro immunomodulating effect of protein-bound polysaccharide, PSK on peripheral blood, regional nodes, and spleen lymphocytes in patients with gastric cancer.

作者信息

Nio Y, Shiraishi T, Tsubono M, Morimoto H, Tseng C C, Imai S, Tobe T

机构信息

First Department of Surgery, Faculty of Medicine, Kyoto University, Japan.

出版信息

Cancer Immunol Immunother. 1991;32(6):335-41. doi: 10.1007/BF01741328.

Abstract

PSK, a protein-bound polysaccharide, has been widely used for cancer immunotherapy in Japan. However, the mechanism of its immunomodulatory effect has not been fully clarified. In the present study the in vitro effect of PSK on the lymphocytes of patients with gastric cancer was studied. Culturing lymphocytes with PSK at 5-100 micrograms/ml increased the level of DNA synthesis, and augmented the cytotoxicities against K562 and KATO-3. Flow-cytometric analysis also showed an increase in the proportion of interleukin-2 (IL-2)-receptor-positive cells after the lymphocytes were cultured with PSK. However the cytotoxicity of cells cultured with PSK was not augmented by the addition of recombinant interferon gamma (rIFN gamma) and rIL-2. Further experiments using fractionated PSK showed that its biological action is present mainly in fractions having molecular masses greater than 10(5) Da. However, these immunomodulations were not seen in all patients. These results suggest that the susceptibility of lymphocytes to PSK may be different in each patients, and that the immunomodulation by PSK may be mediated by mechanisms independent of IFN and IL-2.

摘要

PSK是一种蛋白结合多糖,在日本已被广泛用于癌症免疫治疗。然而,其免疫调节作用机制尚未完全阐明。在本研究中,研究了PSK对胃癌患者淋巴细胞的体外作用。用5 - 100微克/毫升的PSK培养淋巴细胞可提高DNA合成水平,并增强对K562和KATO - 3的细胞毒性。流式细胞术分析还显示,淋巴细胞与PSK培养后,白细胞介素-2(IL - 2)受体阳性细胞的比例增加。然而,添加重组干扰素γ(rIFNγ)和rIL - 2并不能增强用PSK培养的细胞的细胞毒性。使用分级分离的PSK进行的进一步实验表明,其生物学作用主要存在于分子量大于10⁵Da的级分中。然而,并非所有患者都出现这些免疫调节作用。这些结果表明,淋巴细胞对PSK的敏感性在每个患者中可能不同,并且PSK的免疫调节可能由独立于IFN和IL - 2的机制介导。

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The effect of PS-K, a protein bound polysaccharide, on immune responses against allogeneic antigens.
Int J Immunopharmacol. 1983;5(1):35-42. doi: 10.1016/0192-0561(83)90069-3.

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