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γ干扰素、α/β干扰素及肿瘤坏死因子对鼠白血病病毒诱导的肿瘤细胞系中主要组织相容性复合体I类分子的表达有不同影响。

Interferon-gamma, interferon-alpha/beta, and tumor necrosis factor differentially affect major histocompatibility complex class I expression in murine leukemia virus-induced tumor cell lines.

作者信息

Klyczek K K, Murasko D M, Blank K J

机构信息

Department of Microbiology and Immunology, Temple University School of Medicine, Philadelphia, PA 19140.

出版信息

J Immunol. 1987 Oct 15;139(8):2641-8.

PMID:3116091
Abstract

Tumor cell lines induced by Gross murine leukemia virus were examined for cell-surface major histocompatibility complex class I expression. Three of five cell lines constitutively express H-2K and H-2D class I protein. Culturing these cells with interferon (IFN)-gamma, IFN-alpha/beta, or tumor necrosis factor increases both K and D expression in these cell lines. Two of five tumor cell lines express no class I proteins by fluorescence-activated cell sorter analysis, specific immunoprecipitation, and specific hybridization in Northern analysis. Treatment with IFN-gamma induces D, but not K protein expression in one of these cell lines. IFN-alpha/beta and tumor necrosis factor induce neither D nor K expression in this cell line. Thus, these two cytokines appear to have different mechanisms of action than IFN-gamma for altering class I expression. The other class I-negative tumor cell line does not express either K or D proteins under any conditions tested. All five cell lines express beta 2-microglobulin; this expression is increased by IFN-gamma treatment even in cell lines which do not express class I heavy chain. The results of this study demonstrate that 1) different tumor cell lines demonstrate variations in class I gene regulation, and 2) differences in regulation between class I genes may occur within a single cell line.

摘要

对由格罗斯小鼠白血病病毒诱导产生的肿瘤细胞系进行了细胞表面主要组织相容性复合体I类表达的检测。五个细胞系中有三个组成性表达H-2K和H-2D I类蛋白。用γ干扰素(IFN-γ)、α/β干扰素(IFN-α/β)或肿瘤坏死因子培养这些细胞,可增加这些细胞系中K和D的表达。通过荧光激活细胞分选分析、特异性免疫沉淀和Northern分析中的特异性杂交,发现五个肿瘤细胞系中有两个不表达I类蛋白。用IFN-γ处理可诱导其中一个细胞系表达D蛋白,但不表达K蛋白。IFN-α/β和肿瘤坏死因子在该细胞系中既不诱导D蛋白也不诱导K蛋白的表达。因此,对于改变I类表达,这两种细胞因子似乎具有与IFN-γ不同的作用机制。另一个I类阴性肿瘤细胞系在任何测试条件下都不表达K或D蛋白。所有五个细胞系都表达β2微球蛋白;即使在不表达I类重链的细胞系中,IFN-γ处理也会增加其表达。本研究结果表明:1)不同的肿瘤细胞系在I类基因调控方面存在差异;2)在单个细胞系中,I类基因之间可能存在调控差异。

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