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[干扰素诱导肾癌细胞系对淋巴因子激活的杀伤细胞(LAK细胞)的保护作用及酸处理对其敏感性的影响。其与肿瘤细胞上主要组织相容性复合体I类抗原表达的相关性]

[Interferon-induced protection of renal cell cancer cell lines to lymphokine-activated killer (LAK) cells and effect of acid treatment on their susceptibility. Its relevance to expression of major histocompatibility complex class I antigens on tumor cells].

作者信息

Tomita Y, Kimura M, Nishiyama T, Sato S

机构信息

Department of Urology, Niigata University School of Medicine.

出版信息

Nihon Hinyokika Gakkai Zasshi. 1991 May;82(5):762-8. doi: 10.5980/jpnjurol1989.82.762.

Abstract

Renal cell cancer (RCC) cell lines, ACHN and KRC/Y, with or without exposure to interferons (IFNs), were examined for their susceptibility to lymphokine-activated killer (LAK) cells in relation to modulation of major histocompatibility complex (MHC) class I antigens on tumor cells. Flow cytometric analysis demonstrated constitutional expression of class I antigen on both cell lines, which was enhanced by IFN-alpha and -gamma, and was reduced by acid treatment at pH 3. A 4-h 51Cr-release cytotoxicity assay demonstrated that pretreatment of both cell lines with IFN-alpha and -gamma decreased their susceptibility to LAK cells. Although an inverse correlation between class I antigen expression and susceptibility to LAK cells has been reported by others, IFN and acid treatment demonstrated that the degree of class I antigen expression did not correlate with the susceptibility to LAK cells. These results suggest that clinically administered IFNs might induce protection of RCC to LAK cells, and that decrease of susceptibility might depend upon a mechanism different from the enhancement of class I antigens which is frequently expressed on RCC.

摘要

对肾细胞癌(RCC)细胞系ACHN和KRC/Y在暴露或未暴露于干扰素(IFN)的情况下,就肿瘤细胞上主要组织相容性复合体(MHC)I类抗原的调节而言,检测它们对淋巴因子激活的杀伤(LAK)细胞的敏感性。流式细胞术分析表明,两种细胞系上均有I类抗原的组成性表达,其表达被α干扰素和γ干扰素增强,而在pH 3的酸性处理下降低。一项4小时的51Cr释放细胞毒性试验表明,用α干扰素和γ干扰素对两种细胞系进行预处理会降低它们对LAK细胞的敏感性。尽管其他人报道了I类抗原表达与对LAK细胞的敏感性之间呈负相关,但干扰素和酸性处理表明,I类抗原的表达程度与对LAK细胞的敏感性无关。这些结果表明,临床应用的干扰素可能会诱导肾细胞癌对LAK细胞产生保护作用,且敏感性的降低可能取决于一种不同于肾细胞癌上经常表达的I类抗原增强的机制。

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